Spontaneous growth arrest of transformed melanocytes (resulting in benign “moles”) does not result from cell-autonomous oncogene-induced senescence, but can be explained by collective mechanisms used in normal tissue size control.

Environmental cues, not oncogene-induced senescence, may stop melanocytes with an activating mutation in the BRAF gene from turning into melanoma.

A novel master regulatory mechanism of cell proliferation and senscence employs the lncRNA UCA1 and a CAPERα/TBX3 corepressor.

The protein IFI6 regulates DNA replication via the transcription factor E2F2, which is necessary for transformation and growth of melanomas induced by the NRASQ61K mutant oncogene product.

The Yap pathway requires two signals to promote organ growth: a cell intrinsic Hippo signal and a signal induced by injury or inflammation.

Senescent cells are recurrently induced during limb regeneration in salamanders and subsequently eliminated by a highly efficient mechanism of macrophage-dependent surveillance.

Overexpression of TCF7L1 overrides oncogenic Ras-induced senescence, induces cell migration, and promotes growth of skin squamous cell carcinoma independently of its interaction with β-catenin.

Oncogenic BRAF causes genome duplication and reversible growth arrest in human melanocytes that is conditional on microRNA expression and differentiation state.

Late effects of radiation therapy in mice can be prevented by treatment with either senolytics navitoclax or quercetin plus dasatinib or the senostatic metformin.