Pitching the Effects of Cancer as Accelerated Aging

A novel take on the immediate biological consequences of cancer can be found in a recent research brief:

"People think that inflammation drives cancer, but they never understood the mechanism," said Michael P. Lisanti, M.D., Ph.D., Professor and Chair of Stem Cell Biology & Regenerative Medicine at Jefferson Medical College of Thomas Jefferson University and a member of the Kimmel Cancer Center. "What we found is that cancer cells are accelerating aging and inflammation, which is making high-energy nutrients to feed cancer cells."

In normal aging, DNA is damaged and the body begins to deteriorate because of oxidative stress. "We are all slowly rusting, like the Tin-man in the Wizard of Oz," Dr. Lisanti said. "And there is a very similar process going on in the tumor's local environment." Interestingly, cancer cells induce "oxidative stress," the rusting process, in normal connective tissue, in order to extract vital nutrients.

Dr. Lisanti and his team previously discovered that cancer cells induce this type of stress response (autophagy) in nearby cells, to feed themselves and grow. However, the mechanism by which the cancer cells induce this stress and, more importantly, the relationship between the connective tissue and how this "energy" is transferred was unclear.

"Nobody fully understands the link between aging and cancer," said Dr. Lisanti, who used pre-clinical models, as well as tumors from breast cancer patients, to study these mechanisms. "What we see now is that as you age, your whole body becomes more sensitive to this parasitic cancer mechanism, and the cancer cells selectively accelerate the aging process via inflammation in the connective tissue."

You might look back at a recent post on the immune response and aging: increased cancer risk is one of the consequences of a lot of immune system activity and infection throughout life. Likewise, chronic inflammation is a bad thing - it is probably a strong contributing cause to long-term health issues that come with a lot of fat tissue, for example.

Aging itself is no more than accumulated damage of various forms and the flailing of systems trying to adapt to that damage - this realization and the models that result from it are useful. But I think that there is a point at which it stops being useful to talk about accelerated aging, and this is a good example. If you have a strong understanding of a specific process involved in causing damage, then you should be talking about the details and how to use that knowledge to build repair biotechnologies. Aging is far more than just oxidative stress, for example, and labeling this now better understood effect of cancer as accelerated aging just clouds the issue.

The counterpoint to that argument is that talking about accelerated aging caught my eye and made me think about this research and what it might mean. So job well done on the part of Jefferson public relations. I do think that it is in many ways a promising sign that someone in the well-funded field of cancer research is willing to adopt the terminology of aging research and use of accelerated aging as a model in describing their research. It shows that the field of aging research is losing the stigma it had up until comparatively recently - and hopefully in the process becoming exciting once more for younger scientists.


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