A University of Colorado Cancer Center review posits that tissue is the issue regarding cancer frequency and likelihood within older members of the population.
While it has been commonplace to assume that the accrual of cancer-causing mutations is the primary pretext to the increased rate of the disease prevalent in elder adults, the new report debates from behind a more abstract podium — one that attributes the elevated diagnosis quotient with the fluctuating tissue characteristics ubiquitous in the more aged.
"If you look at Mick Jagger in 1960 compared to Mick Jagger today, it's obvious that his tissue landscape has changed," said James DeGregori, PhD, investigator at the University of Colorado Cancer Center and professor of molecular biology at the University of Colorado School of Medicine. "And it's this change, not the accumulation of cancer-causing mutations, that drives cancer rates higher as we grow older."
To substantiate this theory, DeGregori and his counterparts established an evidential parameter composed of four key components.
- The price of puberty — By the time the growth spurt spigot has cooled it’s jets in the late teenage years, a large portion of lifetime mutation accumulation has already occurred. "There's a mismatch between the mutation curve and the cancer curve, meaning that if cancer were due to reaching a tipping point of, say, five or six mutations, we should see higher cancer rates in 20-year-olds, as this is when mutation rate is highest,” DeGregori said.
- Oncogenic optimal — Most healthy tissue is plump with oncogenic mutations, making oncogenes far more popular than the cancers they are trussed to. Thus, as DeGregori articulates, a heightened amount of mutations present in a given system does not necessarily correlate with an amplified level of cancer, neither across the aging population nor in a particular kind of tissue.
- Mono-machines no more — Evolution has fomented a transition in the human race, where people have gone from being one-celled organisms with short life spans to multicellular, long-lived beings that require more complicated machinery to ward off disease whilst upholding tissues. "But we're no better at preventing mutations than our yeast or bacteria cousins," DeGregori says. "You'd think if avoiding mutations was key to avoiding cancer, we'd be better at it than we are."
- Stemming from stem cells — “Stem cells harboring the oncogenes tend to get weeded out," said DeGregori when prompted about studies performed on mice, where oncogenes were introduced into stem cells and should have aided instead of impeded stem cell survival.
It’s more about the mechanism of youth slowly giving way with age than the build-up of mutations that cause cancer to propagate within older individuals, DeGregori concluded.
"It's like what happened to the dinosaurs 65 million years ago," he said. "Dinosaurs were great and they weren't changing that fast — they were well adapted to their landscape. Until that darn meteor. Suddenly what was fit was no longer fit. The species didn't have to change their mutation rate — it was the new landscape that drove speciation. Similarly, what primarily drives cancer rates higher as we age is the changed landscape."
"When tissue is old, healthy cells are no longer a perfect fit, and mutations might help a cancer cell adapt in ways a healthy cell can't," DeGregori added.
When tissue ages, cancer cells are allowed the opportunity to outcompete the normal healthy cells that have fallen past their prime. It’s a new Icarus theory to ponder — a big bang and a long fall from the top tier of the survivalist’s ladder.