ABSTRACT
One of the most visible signs of chronological aging for humans involves fairly
obvious clinical changes in which the aged skin appears wrinkled, saggy, dis-
colored (1), and is more frequently associated with various types of cancer (2).
Additional characteristics of the aging phenotype is skin include wound healing
defects, decreased skin thickness with less subcutaneous fat tissue, and hair loss.
Skin aging represents a complex process involving both intrinsic aging as well as
extrinsic aging (3). For the most part in simplistic terms, intrinsic skin aging
results primarily from genetically programmed molecular and cellular events in
which there is progressive telomere shortening involving the ends of DNA;
whereas extrinsic aging relates more to environmentally induced cellular
changes in which there is more widespread DNA damage, accelerated telomere
shortening, and a key role for p53 and related genes (4-6). A detailed review of
the complexities of intrinsic and extrinsic skin aging is beyond the scope of this
article (7), rather the focus will be on the relative biological consequences by
which senescent cell types in the skin (particularly epidermal keratinocytes and
dermal fibroblasts) may impact (either positively or negatively) the development
of skin cancer.
