~ Cancer and Aging Links
LIFE EXTENSION UPDATE EXCLUSIVE:
Cancer and Aging Link Explained
The relationship between aging and major diseases seems like an obvious one. Life extensionists have long contended that aging may be the cause of diseases that occur later in life. Individual cells, too, experience aging. Interestingly, the arrested growth and altered function of cells known as cellular senescence is believed to suppress the formation of tumors in early life.
However, in a study to be published in the journal Proceedings of the National Academy of Sciences (http://www.pnas.org/), researchers at Lawrence Berkeley Laboratory found that senescent human fibroblasts cause epithelial cells to proliferate and form tumors.
Cellular senescence is an example of antagonistic pleiotropy, a term used to describe genetic traits that have differing effects. A trait genetically selected to enhance early life can have adverse effects later in life.
Dividing cells experience a gradual shortening of telomeres, DNA that exists at the end of chromosomes, which causes a senescence response. Ceullular senescence is similar to apoptosis, which prevents the growth of cells at risk for transformation into cancer cells. Yet their accumulation with age may contribute to age-related tissue function decline, and because they can alter tissue microenvironment they may be partly responsible for the dramatic age-associated increase in cancer.
The researchers in this study cocultured epithelial cells from three human and and one mouse cell line with presenescent as well as senescent connective tissue cells known as fibroblasts. Three of the lines were considered prmalignant, having some cancer-predisposing mutations, and one was an aggressive human breast cancer cell line.
Senescent fibroblasts stimulated the growth of all four cell lines to a much greater extent than those which were presenescent. Normal human epithelial cells were also tested, but their growth was not affected by either group of fibroblasts.
To test the tumor-promoting ability of senescent cells in vivo, premalignant epithelial cells in combination with presenescent, senescent, immortalized, or no fibroblasts were injected into immunocompromised mice. The incidence and size of tumors that later developed was significantly greater in the mice who received the senescent cells than in those who received presenescent cells. When weakly tumorigenic and aggressive malignant epithelial cells were tested, senescent fibroblasts further accelerated the development of tumors in both lines.
The researchers speculate that the growth arrest known as senescence was genetically selected to ensure that damaged cells at risk of turning into cancer cells do not proliferate. As these cells are rarer in younger organisms, the changes they cause have little impact, but as these cells accumulate with age, their influence becomes more significant. Their results suggest a link between cancer and aging and a method by which genetic and epigenetic events synergize to create this link.
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