A pathway directed by the KRAS oncoprotein leads to aberrant hypermethylation and transcriptional silencing of many genes including tumor suppressors, thereby promoting tumor development.

Evolution of tumor suppressor genes can involve a trade-off because the acquisition of certain anti-cancer characteristics diminishes the ability to regenerate damaged tissue.

The functional relevance of stem cell niche perturbation in sarcomagenesis is defined and the mouse model presented provides a rationale for the use of combination therapy for the treatment of genetically heterogeneous sarcomas.

Aging is associated with stress-induced senescence of adipose stromal cells, leading to impaired adipogenesis, oxidative stress, mitochondrial dysfunction, and insulin resistance, all being alleviated by metformin treatment of adipose stromal cells.

Application of a live-cell reporter for CDK4/6 activity reveals rapid activity changes and reversibility in the cell-cycle entry signaling program.

The study of embryo-endometrial interactions in assembloid co-cultures identifies novel mechanisms of reproductive failure.

While acute senescence of decidualizing cells drives the inflammatory response underpinning uterine receptivity, subsequent clearance by activated natural killer cells transiently rejuvenates the cycling endometrium, enabling transition into a gestational tissue upon embryo implantation.

A mouse model reveals that a p53 SNP impacts longevity via modulating the balance of cancer risk and the self-renewal function of stem/progenitor cells, which supports a role of p53 in regulation of longevity.

Ablation of the Cdkn1c cell cycle inhibitor leads to defective muscle stem cell dynamics and myogenic potential, while progressive cytoplasmic to nuclear cellular localization of the Cdkn1c protein regulates growth arrest.