Looking at the length of telomeres — the protective caps on the end of chromosomes that protect the DNA inside — scientists from Northwestern University and Harvard University have developed a technique that could one day result in a diagnostic test for cancer years ahead of time.

Mounting evidence is finding telomeres are responsible for more than just chronological aging. As cells divide and multiply, the telomeres lose some length to make up for the added chromosomes. But in that normal shortening they can activate destructive bodily processes, which may lead to disease. New evidence suggests the rate at which they shorten is also important for understanding future development of cancer.

Publishing in the journal EBioMedicine, researchers found distinct patterns in people’s telomeres in the lead up to formal diagnosis. Initially, people with cancer seemed to be 15 years older, chronologically, than people without cancer — an indication their telomeres were quickly wasting away. But then three or four years before diagnosis, that shortening stopped.

"We saw the inflection point at which rapid telomere shortening stabilizes," said the study’s lead author Dr. Lifang Hou in a statement. “We found cancer has hijacked the telomere shortening in order to flourish in the body.”

In total, Hou and her colleagues tracked 792 people over a period of 13 years, from 1999 to 2012. By the end of the study, 135 people had developed various types of cancer. Their findings suggest blood telomere length, or BTL, may be able to tip off scientists and doctors about risks people may face later on.

"We were able to take advantage of the fact that the same people came in for follow-up visits multiple times," Hou told Medical Daily. "For example, if someone comes in in 2010 and reports that they were diagnosed with cancer, we can go back to their visit in 2002 and flag them as 'developing cancer.'"

The team hopes to use that information in developing a method of stopping the cancer cells from eating away at people’s BTL. And to do that, future tests would need to figure out how, exactly, the hijacking happens. Hou and her colleagues are expanding their research to see how women and people of other ethnicities get affected by the same processes. "In addition, we are also currently working on studies of traditional cancer risk factors (e.g., obesity/physical activity) and how they interact with telomeres to increase cancer risk."

Recently, other research has offered its own interpretation of telomere-mediated disease. A study published in the journal Nature Genetics found genetic causes made some people’s telomeres longer than others. These varying lengths predisposed subjects to pathological disease, including several cancers and idiopathic pulmonary fibrosis.

The latest study builds on this kind of research to home in on cancer specifically, Hou says. Cancer treatment can lead to telomere shortening in addition to the cancer itself. "This likely explains why the previous studies have been so inconsistent." Without a definite timeline for when telomeres begin to shorten in response to cancer cell activity, scientists are left without any causal information.

"Long-term, it would be great to see this research turned into a way to detect cancer earlier than we do now."

Source: Hou L, Joyce B, Gao T, et al. Blood Telomere Length Attrition and Cancer Development in the Normative Aging Study Cohort. EBioMedicine. 2015.