Telomere biomarker may lead to blood test that predicts cancer years in advance
A DISTINCT pattern of changes in blood telomeres appears to predict cancer years before diagnosis. This was the result of a new study believed to be the first to follow what happens to the protective ends of DNA strands over time in people who go on to develop cancer.
Researchers from Northwestern and Harvard Universities report their findings in the new journal EBioMedicine. They found blood telomeres age faster and then stop aging for a few years in the period leading up to a cancer diagnosis.
Lead author Lifang Hou, associate professor in Preventive Medicine – Cancer Epidemiology and Prevention at Northwestern University Feinberg School of Medicine, says: “Understanding this pattern of telomere growth may mean it can be a predictive biomarker for cancer.”
Telomeres are sequences of DNA on the ends of chromosomes – like the plastic caps on the ends of shoelaces – that stop them fraying and losing their integrity.
They gradually shorten as we age – by the time we grow up they are half the length they were when we were born, then they halve again as we enter old age.
Rapid shortening of telomeres followed by three to four years of stabilization Scientists consider blood telomeres to be a marker of biological age, but they have also been looking at how they change in people developing cancer.
However, studies exploring blood telomere changes in relation to cancer have reached inconsistent conclusions: some say people developing cancer have shorter blood telomeres, others say they are longer, and some find no links at all.
In the new study, the team investigated how telomeres change over time as opposed to taking just a single snapshot. They found that a distinct pattern in the changing length of blood telomeres can predict cancer years before people are diagnosed.
The distinctive pattern shows a rapid shortening of the blood telomeres followed by three to four years where not much happens to the length. The researchers say this distinctive pattern could serve as a biomarker that predicts cancer development with a blood test.
As far as they know, theirs is the first study to report how telomere length changes in the years leading up to a cancer diagnosis, before treatment begins.
This is significant because treatment for cancer can affect telomere length. For their study, the researchers measured telomere length several times over a 13-year period in 792 people.
One hundred and thirty-five of the participants eventually developed various cancers, including leukemia, and prostate, skin and lung cancer. The telomeres of the participants who were later diagnosed with cancer aged much faster – that is they shortened more rapidly – in the first few years.
In the participants who developed cancer, the telomeres looked as much as 15 years older than those of the participants who did not develop cancer.
But what was surprising was that the accelerated aging stopped three to four years before cancer diagnosis. Prof. Hou adds: “Because we saw a strong relationship in the pattern across a wide variety of cancers, with the right testing these procedures could be used to eventually diagnose a wide variety of cancers.”
She explains that the inconsistency of previous findings may be because they did not spot the stabilizing period: “We saw the inflection point at which rapid telomere shortening stabilizes. We found cancer has hijacked the telomere shortening in order to flourish in the body.”
Telomeres shorten every time a cell divides, which is why they get progressively shorter as we age. If the telomeres of a cell become too short, they can cause the cell to become faulty, and normally the cell self-destructs.
This raises a puzzling scientific question: since cancer cells divide more rapidly than normal cells, why don’t they self-destruct when their telomeres become dangerously short? This study may have the answer: it suggests cancer cells have found a way somehow to stop telomeres getting shorter.
Prof. Hou says if we can find out how cancer cells hijack this normal cell process, then perhaps we can develop treatments that cause them to self-destruct without harming healthy cells.