Peter D. Adams

TL;DR: It is shown, in a humanized genetically-modified mouse model of pancreatic ductal adenocarcinoma (PDAC), that autophagy’s role in tumour development is intrinsically connected to the status of the tumour suppressor p53, and treatment with hydroxychloroquine significantly accelerates tumour formation in mice containing oncogenic Kras but lacking p53.

TL;DR: The study suggests that this new function of autophagy acts as a guarding mechanism protecting cells from tumorigenesis, and prevents activated RAS-induced lamin B1 loss and attenuates oncogene-induced senescence in primary human cells.

TL;DR: The results suggest that mitochondria are a candidate target for interventions to reduce the deleterious impact of senescence in ageing tissues.

TL;DR: Key challenges to understand clock mechanisms and biomarker utility are discussed, including dissecting the drivers and regulators of age-related changes in single-cell, tissue- and disease-specific models, as well as exploring other epigenomic marks, longitudinal and diverse population studies, and non-human models.

TL;DR: Comparing genome-wide Lys4 trimethylation on histone H3 and H3K27me3 distributions between proliferating and senescent human cells found dramatic differences in senescence, suggesting that pre-malignant senescent chromatin changes foreshadow epigenetic cancer changes.