Abstract
Cancer shows a strong association with aging and prognosis in aged individuals is usually poor. A widely accepted paradigm attributes this phenomenon to the accumulation of oncogenic mutations over time. While independently associated with age, mutually exclusive mutations BRAF and NRAS encompass nearly 75% of all cases in melanoma. Furthermore, these mutations alone are usually insufficient for tumor initiation. Nevi harboring activating mutations infrequently progress to melanoma due to oncogene-induced senescence. Given that the incidence of melanoma increases after the age of 55 according to the SEER (Surveillance, Epidemiology and End Results Program) database, do age-dependent alterations in the tissue landscape act upon pre-existing mutations leading to melanomagenesis? A recent study by Kaur et al. published in Nature provides new insight into how fibroblasts in an aging microenvironment can in part contribute to melanoma progression. This article is protected by copyright. All rights reserved.
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CITATION STYLE
Teh, J. L. F. (2016). Frizzled with age: an opportunity for ‘gerontological medicine.’ Pigment Cell & Melanoma Research, 29(5), 488–489. https://doi.org/10.1111/pcmr.12493
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