DNA's protective cap linked with lung cancer

Scientists have linked long telomere - protective caps of DNA that prevent damage to the ends of chromosomes - with an increased lung cancer risk among people.

New York: Scientists have linked long telomere - protective caps of DNA that prevent damage to the ends of chromosomes - with an increased lung cancer risk among people.

The large-scale genetic study, however, did not observe any significant association between telomere length and other cancer types or subtypes.

"Our work provides compelling evidence of a relationship between long telomeres and increased risk for lung adenocarcinoma (a form of cancer)," said study leader Brandon Pierce, assistant professor of public health sciences at the University of Chicago.

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.

For the study, the team used a novel method to measure genetic predisposition for telomere length rather than physiological measures which are confounded by factors such as age and lifestyle.

They used genome data from more than 50,000 cancer cases and 60,000 controls through the GAME-ON (Genetic Associations and Mechanisms in Oncology) network.

The team compared telomere lengths with the risk of developing breast, lung, colorectal, ovarian and prostate cancers, including subtypes.

They found that longer telomeres were significantly associated with increased risk for lung cancer - specifically lung adenocarcinoma, which more than doubled in risk for every 1000 base pair increase in telomere length.

A portion of the telomere DNA is lost during cell division.

This leads to telomere shortening over time, which has been thought of as a time-delay "fuse" that can trigger cell death or genomic instability.

Shortened telomeres have been implicated in ageing and cardiovascular diseases, but their relationship with cancer risk was unclear so far.

The team is now examining telomere length in additional populations to evaluate whether some groups based on age, gender, smoking history and other factors may be at additional increased risk.

The findings were published in the journal Human Molecular Genetics.

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