Stimulation of epidermal hyperplasia and tumorigenesis by resident p16INK4a-expressing cells

Narmen Azazmeh; Ittai Ben-Porath

doi:10.1080/23723556.2020.1819752

Stimulation of epidermal hyperplasia and tumorigenesis by resident p16^INK4a-expressing cells

Narmen Azazmeh, Ittai Ben-Porath^*

^*Corresponding author for this work

Department of Developmental Biology and Cancer Research

Research output: Contribution to journal › Comment/debate

1 Scopus citations

Abstract

p16^INK4a (CDKN2A) is a central tumor-suppressor and activator of senescence. We recently found that prolonged expression of p16^INK4a in epidermal cells induces hyperplasia and dysplasia through Wnt-mediated stimulation of neighboring keratinocytes. The study suggests a pro-tumorigenic function of p16^INK4a in early epidermal lesions, which could potentially be targeted by senolytic therapy.

Original language	American English
Article number	1819752
Journal	Molecular and Cellular Oncology
Volume	7
Issue number	6
DOIs	https://doi.org/10.1080/23723556.2020.1819752
State	Published - 1 Nov 2020

Bibliographical note

Funding Information:
This study was supported by grants from the Israel Science Foundation (1009/13, 2092/18) and from the DKFZ-MOST Fund (CA-161) (I.B.), and by a fellowship from the Israel Council for Higher Education (N.A.)

Publisher Copyright:
© 2020 The Author(s). Published with license by Taylor & Francis Group, LLC.

Keywords

CDKN2A
P16
Wnt
aging
epidermis
senescence

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1080/23723556.2020.1819752

Cite this

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title = "Stimulation of epidermal hyperplasia and tumorigenesis by resident p16INK4a-expressing cells",

abstract = "p16INK4a (CDKN2A) is a central tumor-suppressor and activator of senescence. We recently found that prolonged expression of p16INK4a in epidermal cells induces hyperplasia and dysplasia through Wnt-mediated stimulation of neighboring keratinocytes. The study suggests a pro-tumorigenic function of p16INK4a in early epidermal lesions, which could potentially be targeted by senolytic therapy.",

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AU - Ben-Porath, Ittai

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N2 - p16INK4a (CDKN2A) is a central tumor-suppressor and activator of senescence. We recently found that prolonged expression of p16INK4a in epidermal cells induces hyperplasia and dysplasia through Wnt-mediated stimulation of neighboring keratinocytes. The study suggests a pro-tumorigenic function of p16INK4a in early epidermal lesions, which could potentially be targeted by senolytic therapy.

AB - p16INK4a (CDKN2A) is a central tumor-suppressor and activator of senescence. We recently found that prolonged expression of p16INK4a in epidermal cells induces hyperplasia and dysplasia through Wnt-mediated stimulation of neighboring keratinocytes. The study suggests a pro-tumorigenic function of p16INK4a in early epidermal lesions, which could potentially be targeted by senolytic therapy.

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KW - Wnt

KW - aging

KW - epidermis

KW - senescence

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