There is no question that the complex biological processes of aging and cancer are
inter-related [
[1]
]. As cancer incidence increases with aging in many organ systems exposed to environmental
factors such as ultraviolet-light and the skin, it is not surprising that investigators
have been probing for mechanistic insights linking aging, cellular senescence, and
tumorigenesis. However, the primary focus of these previous studies has been on asking
how senescent cells might promote cancer, or how malignant cells bypass replicative
senescence [
[1]
]. Since the biology of senescence has been most well studied in fibroblasts dating
back to the pioneering studies of Hayflick, investigators have made steady progress
in defining the phenotype of senescent stromal cells such as fibroblasts. Senescent
fibroblasts were found to resemble activated, or carcinoma-associated fibroblasts,
suggesting that a microenvironment may be present in aged tissue conducive to cancer
progression. More recently, Campisi and coworkers extended these findings by demonstrating
that senescent fibroblasts can stimulate growth and tumorigenic transformation of
premalignant cells in vitro and in vivo [
[2]
].To read this article in full you will need to make a payment
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References
- Cancer and ageing: rival demons?.Nat Rev Cancer. 2003; 3: 339-349
- Senescent fibroblasts promote epithelial cell growth and tumorigenesis: a link between cancer and aging.Proc Natl Acad Sci USA. 2001; 98: 12072-12077
- Escaping the stem cell compartment: sustained UVB exposure allows p53-mutant keratinocytes to colonize adjacent epidermal proliferating units without incurring additional mutations.Proc Natl Acad Sci USA. 2001; 98: 13948-13953
- A biomarker that identifies senescent human cells in culture and in aging skin in vivo.Proc Natl Acad Sci USA. 1995; 92: 9363-9367
- Tumor suppressor maspin is up-regulated during keratinocyte senescence, exerting a paracrine antiangiogenic activity.Cancer Res. 2004; 64: 2956-2961
- Spontaneous malignant transformation of human ovarian surface epithelial cells in vitro.Clin Cancer Res. 2001; 7: 4280-4287
- Cellular senescence as a tumor-suppressor mechanism.Trends Cell Biol. 2001; 11: S27-S31
- Id-1 delays senescence but does not immortalize keratinocytes.J Biol Chem. 2000; 275: 27501-27504
- Defects in TGF-beta signaling overcome senescence of mouse keratinocytes expressing v-Ha-ras.Oncogene. 2000; 19: 1698-1709
- Apoptosis in proliferating, senescent, and immortalized keratinocytes.J Biol Chem. 1999; 274: 23358-23367
Article info
Publication history
Received:
October 15,
2004
Identification
Copyright
© 2005 Japanese Society for Investigative Dermatology. Published by Elsevier Inc. All rights reserved.
