As a study concludes that long telomeres are significantly associated with an increased risk for lung cancer, their relationship with cancer becomes more complicated.
Telomeres are perhaps the most publicised symbol in the aging debate; they're memorable and easier to understand in comparison to some of the more complicated hallmarks of aging. A considerable amount of research now also suggests they are either a key factor or symptom of the aging process, and that repairing them could well have restorative, therapeutic effects.
While it would be wonderful to have stumbled upon an elegant and simple aging 'switch', telomere biology has been controversial from the start. Cancer needs to protect its telomeres in order to expand indefinitely and the relationship between cancer and telomere length is apparently a complicated one. We know that short telomeres have been consistently linked with genomic instability (DNA becoming unstable and prone to mutation, like a shoelace unraveling without a cap) which can facilitate senescence (essentially old cells that no longer divide), inflammation and may contribute to raising cancer risk. Shortening telomeres also might protect against harmful mutations building up over time. While in mice, increasing activity of the enzyme telomerase (which rebuilds telomeres) proved immensely beneficial and was not associated with an increase in cancer risk, the case for humans is not established. Mice after all begin life with longer telomeres than humans do and yet live barely any time at all, making them a relatively poor model for human aging.
“The prevailing hypothesis has been that short telomeres are bad for health, but it appears that this does not necessarily translate to some types of cancer”
While It's tempting to hope for a simple, unifying solution to a problem, these are rare when it comes to biology. Interfering with some biological processes can often prove disastrous, leaving you with a worse problem than you started with. Attempting to hit a disease with a drug that inhibits the activity of a particular protein for example might well do just that, but the system might tune up production of something else to compensate. Because of this, often multiple drugs are required to fix the side effects of another.
While the study's findings do make things more complicated, there are a few important things to think about:
- Only lung cancer, and prostate cancer to some extent, showed an increase in risk along with telomere length. This is unfortunate, but it shows that telomeres in themselves are potentially less connected to cancer as a whole than was previously feared. If they posed a significant risk across the board, then more types would probably have been correlated.
- The length was a factor but not in comparison to original length. It may be that there is an ideal zone and that extending telomeres too much can be just as detrimental as having short ones. Extending intermittently back to a youthful profile from time to time might therefore have a beneficial effect, without lengthening persistently and increasing risk of cancer.
'The team suggests a potential explanation for this observation is that long telomeres enable more rounds of cell division than short telomeres, which could allow cells to live longer and have more opportunities to accumulate carcinogenic mutations.'
While great strides have been made, the fact is we simply don't know enough yet about the intricacies of the aging process to make strong judgements. Studies like this remind us to keep an open mind and that biology often turns out to be more complicated than you predict. Shortened telomeres may well play a part in the aging process, but there may be other factors playing a larger role.
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