Why cancer rate increases with age (it's not what you think)

July 2, 2012

Cancers are age-related, much more frequent in the old than in the young. A University of Colorado Cancer Center review published today in the journal Oncogene argues against the conventional wisdom that the accumulation of cancer-causing mutations leads to more cancer in older people, instead positing that it is the changing features of tissue in old age that promote higher cancer rates in the elderly.

"If you look at Mick Jagger in 1960 compared to Mick Jagger today, it's obvious that his tissue landscape has changed," says James DeGregori, PhD, investigator at the University of Colorado Cancer Center and professor of at the University of Colorado School of Medicine. "And it's this change, not the accumulation of cancer-causing , that drives cancer rates higher as we grow older."

For evidence, DeGregori points first to the fact that by the time we stop growing in our late teens, we've already accumulated a large fraction of the mutations we will have in our lifetimes. "There's a mismatch between the mutation curve and the cancer curve," DeGregori says, 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.

Second, DeGregori points out that even healthy tissues are full of oncogenic mutations. "These mutations are many times more common than the cancers associated with them," DeGregori says. Simply, more mutations doesn't equal more cancer – not across the aging population and not even in specific tissues.

DeGregori's final two points come from evolution. As we've evolved from one-celled, short-lived life forms into multicellular, long-lived humans, we've had to develop complicated machinery to maintain our tissues and avoid disease.

"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."

And finally, if these oncogenes were the evil super-villains they've been made out to be, capable of taking over surrounding tissue, then introducing oncogenes into mice stem cells should help rather than hurt these cells' survival. "Rather, stem cells harboring the oncogenes tend to get weeded out," says DeGregori.

Instead of gathering mutations until they give us cancer, DeGregori says that as we age, the mechanisms that younger adults use to fight cancer, deteriorate.

"It's like what happened to the dinosaurs 65 million years ago," DeGregori says. "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 – it was the new landscape that drove speciation. Similarly, what primarily drives higher as we age is the changed landscape."

Our healthy cells are optimized for the conditions of our healthy, younger tissue. Change this balance, as does an oncogenic mutation, and they're no longer a perfect fit for the surroundings – healthy cells in young bodies quickly outcompete cells with cancerous mutations.

But, "when tissue is old, are no longer a perfect fit, and mutations might help a cancer cell adapt in ways a healthy cell can't," DeGregori says.

Blot out the sun with a meteor's cloud of dust and mammals will eventually outcompete thunder lizards; age tissue past the expiration date evolution's set and cells can outcompete their normal but aged peers.

Explore further: Study identifies pathway to enhance usefulness of EGFR inhibitors in lung cancer treatment

Related Stories

Study identifies pathway to enhance usefulness of EGFR inhibitors in lung cancer treatment

June 29, 2012
Many lung cancers are driven by mutations in the epidermal growth-factor receptor (EGFR), and so it makes sense that many successful modern treatments block EGFR activity. Unfortunately, cancers inevitably evolve around EGFR ...

Study pinpoints and plugs mechanism of AML cancer cell escape

January 18, 2012
A study published this week in the journal Leukemia identifies a mechanism that acute myeloid leukemia (AML) cells use to evade chemotherapy – and details how to close this escape route.

Recommended for you

Researchers identify gene variants linked to a high-risk children's cancer

September 25, 2017
Pediatric researchers investigating the childhood cancer neuroblastoma have identified common gene variants that raise the risk of an aggressive form of that disease. The discovery may assist doctors in better diagnosing ...

Prostaglandin E1 inhibits leukemia stem cells

September 25, 2017
Two drugs, already approved for safe use in people, may be able to improve therapy for chronic myeloid leukemia (CML), a blood cancer that affects myeloid cells, according to results from a University of Iowa study in mice.

Cancer vaccines need to target T cells that can persist in the long fight against cancer

September 25, 2017
Cancer vaccines may need to better target T cells that can hold up to the long fight against cancer, scientists report.

Lung cancer treatment could be having negative health effect on hearts

September 25, 2017
Radiotherapy treatment for lung cancer could have a negative effect on the health of your heart new research has found.

MRI contrast agent locates and distinguishes aggressive from slow-growing breast cancer

September 25, 2017
A new magnetic resonance imaging (MRI) contrast agent being tested by researchers at Case Western Reserve University not only pinpoints breast cancers at early stages but differentiates between aggressive and slow-growing ...

Alternative splicing, an important mechanism for cancer

September 22, 2017
Cancer, which is one of the leading causes of death worldwide, arises from the disruption of essential mechanisms of the normal cell life cycle, such as replication control, DNA repair and cell death. Thanks to the advances ...

0 comments

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.