In:
Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 93, No. 24 ( 1996-11-26), p. 14025-14029
Abstract:
The multiple genetic hit model of cancer predicts that normal
individuals should have stable populations of cancer-prone, but noncancerous, mutant cells awaiting further genetic hits. We report
that whole-mount preparations of human skin contain clonal patches of p53-mutated keratinocytes, arising from the dermal–epidermal junction
and from hair follicles. These clones, 60–3000 cells in size, are present at frequencies exceeding 40 cells per cm 2 and
together involve as much as 4% of the epidermis. In sun-exposed skin, clones are both more frequent and larger than in sun-shielded skin. We
conclude that, in addition to being a tumorigenic mutagen, sunlight acts as a tumor promoter by favoring the clonal expansion of
p53-mutated cells. These combined actions of sunlight result in normal individuals carrying a substantial burden of keratinocytes predisposed
to cancer.
Type of Medium:
Online Resource
ISSN:
0027-8424
,
1091-6490
DOI:
10.1073/pnas.93.24.14025
Language:
English
Publisher:
Proceedings of the National Academy of Sciences
Publication Date:
1996
detail.hit.zdb_id:
209104-5
detail.hit.zdb_id:
1461794-8
SSG:
11
SSG:
12
Permalink