Age Inhibits Cancer Development

The human aging process may impede cancer development, according to the findings of a recent study published in Aging Cell.

In this study, researchers utilized data from the Genotype‐Tissue Expression (GTEx) Project and The Cancer Genome Atlas (TCGA) to compare genes differentially expressed with age and genes differentially expressed in cancer among nine human tissues.

According to their findings, in most tissues, aging and cancer gene expression patterns changed in the opposite direction, suggesting that age hinders cancer progression. An exception was found in thyroid and uterus cancers, where researchers observed changes transcriptomic changes in the same direction, indicating cancer development with age. Moreover, the researchers observed that cellular senescence signatures changed directions as aging in human tissues aged and in the opposite direction of cancer signatures.

“One of the reasons our bodies have evolved to have senescent cells is to suppress cancers. But then it seems that senescent cells accumulate in aged human tissues and may contribute to ageing and degeneration,” said Dr. Joao Pedro De Magalhaes from the University of Liverpool’s Integrative Genomics and Ageing Group said in a press release. “Importantly, our work challenges the traditional view concerning the relationship between cancer and ageing and suggests that ageing processes may hinder cancer development.”

Dr. De Magalhaes, the study’s lead researcher added that “while mutations accumulate with age and are the main driver of cancer, ageing tissues may hinder cell proliferation and consequently cancer. So, you have these two opposite forces, mutations driving cancer and tissue degeneration hindering it. This may explain why at very advanced ages cancer incidence levels off and may even decline.”

“Our results highlight the complex relationship between ageing, cancer and cellular senescence and suggest that in most human tissues ageing processes and senescence act in tandem while being detrimental to cancer,” Dr. De Magalhaes concluded. “But more mechanistic studies are now needed.”