Common Delayed Senescence of Melanocytes from Multiple Primary Melanoma Patients

Jaskaren S Kohli,Elena Tolomio,Simona Frigerio,Andrea Maurichi,Monica Rodolfo,Dorothy C Bennett

doi:10.1016/j.jid.2016.10.026

Abstract

Common Delayed Senescence of Melanocytes from Multiple Primary Melanoma Patients

Highlights

Mutations in other senescence-related genes have been identified in familial melanoma: TERT, CDK4, and genes encoding components of the telomeric cap shelterin, for example POT1, and TERF2IP (Aoude et al, 2015a; Robles-Espinoza et al, 2014; Shi et al, 2014). These observations suggested that multiple primary melanoma (MPM) may commonly be associated with genetically defective or delayed melanocyte senescence
This hypothesis has been tested by explanting melanocyte cultures from biopsy samples of sun-protected normal skin from MPM or single primary melanoma (SPM) patients who are wild type for known melanoma-associated mutations other than in MC1R
Melanocyte culture lifespans for each patient are included in Supplementary Table S1

Summary

Introduction

Common Delayed Senescence of Melanocytes from Multiple Primary Melanoma Patients Journal of Investigative Dermatology (2017) 137, 766e768; doi:10.1016/j.jid.2016.10.026 CDKN2A, the most common known familial melanoma gene, encodes p16, a broad-spectrum tumor suppressor and mediator of cell senescence (Aoude et al, 2015b; Bennett, 2016). P16 induces senescence by inhibiting CDK4-mediated phosphorylation of retinoblastoma-family proteins, resulting in retinoblastoma proteins binding and repressing E2F transcription factor activity, which is needed for S-phase entry in the cell cycle (Bennett, 2016).

Results

Conclusion