By Lodovico Balducci (Editor), Martine Extermann (Editor)
Organic foundation of Geriatric Oncology highlights learn concerns which are particular to geriatric oncology within the box of carcinogenesis and melanoma prevention and remedy, in response to the biologic interactions of melanoma and age. It illustrates the advantage of the rules of geriatrics within the administration of melanoma within the older person. This quantity presents a body of reference for practicioners of any specialties desirous about the administration of older sufferers and for oncologists keen on the administration of melanoma of older participants. it's a resource for uncomplicated and scientific scientists exploring the interactions and rising details of melanoma and getting older.
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Sample text
Eur J Cancer 2001; 37:S114S117 70. Ponten J: Cell biology of precancer. Eur J Cancer 2001; 37:S97-S113 71. Vijg J: Somatic mutations and aging: a re-evaluation. Mutat Res. 2000; 447:117-135 72. Matoha HF; Cosgrove JW; Atak JR; Rapoport SI: Selective elevation of c-myc transcript levels in the liver of the aging Fischer-344 rat. Biochem Biophys Res Commun 1987; 147:1-7 73. Ono T; Uehara Y; Kurishita A; Tawa R; Sakurai H: Biological significance of DNA methylation in the aging process. Age & Aging 1993; 22:534-543 74.
Age is considered as a variable because older cells may already present in advanced carcinogenic stages, are primed to the effects of environmental carcinogens and consequently may develop cancer more rapidly and at higher rate when exposed to these substances. A number Figure 3. The multistage carcinogenesis inducted by single exposure to a carcinogenicagent at different ages. BIOLOGICAL INTERACTIONS 23 of factors, including genetic predisposition, oxidative stress, and previous exposure to carcinogens may be responsible of the molecular changes that prime aging cells to environmental carcinogens.
The character of these changes could vary in different tissues and might cause uneven tissue aging. Dolle et al. 88 using a lacZ plasmid transgenic mouse model, determined spectra of spontaneous point mutations in different organs in young and old mice. While similar at a young age, the mutation spectra among these organs were significantly different in old age. The authors stressed that the replicative history per se is not the underlying causal factor of age-related organ-specific differences in mutations spectra.