UK Biobank data reveals new associations between smoking and lung cancer

Health and genetic data from the UK Biobank has revealed new genetic associations between smoking and lung cancer, including five areas of DNA for the first time associated with heavy smoking.

The study, led by Professor Ian Hall from the University of Nottingham and Professor Martin Tobin from the University of Leicester, looked at the lung health of around 500,000 participants in the UK Biobank. From this group, the researchers analysed the genetic data from around 50,000 who had been selected on the basis of their lung health and whether or not they were smokers.

Using a new genotyping array to measure over 800,000 genetic variants in each sample, the researchers compared lung health and smoking behaviour with genetic variations across the whole human genome. They identified genetic differences that could affect the likelihood that someone will smoke, as well as being associated with different levels of lung health in both people that smoke and those that do not.

In particular, the findings could explain why some people who have smoked all their lives appear to have healthy lungs. It suggests that smokers who live into their old age may possess mutations in their DNA that affects the way lungs respond to damage, such as that caused by smoking.

The Medical Research Council, which funded the research, believes these findings could lead to the development of treatments to improve lung function, reports BBC News.

The study, which involved researchers from the UK BiLEVE, UK Lung Exome Variant Evaluation, also identified six genetic variants associated with lung health and chronic obstructive pulmonary disease (COPD), the third leading cause of death worldwide. Five variants were associated with heavy smoking.

'These findings, taken together with previous findings, will help define pathways underlying predisposition to development of COPD and smoking behaviours', the authors said.

The researchers explain that understanding the genetic basis of airflow obstruction and smoking behaviour is important to identifying the mechanisms that cause COPD.  They believe that the findings may one day support research into new treatments for diseases, such as COPD.

'Smoking is the biggest lifestyle risk factor for COPD. Many, but not all, smokers develop the disease', said Professor Tobin.

'Genetics play a big part, as they do in smoking behaviour. Our research helps to tell us why, paving the way for improved prevention and treatment'.

However, he stressed that the findings did not mean people should avoid giving up smoking. 'Stopping smoking is the best way to prevent smoking-related diseases such as COPD, cancers and heart disease', he said.

Dr David Crosby, of the MRC, said: 'Thanks to the 500,000 people who have volunteered to make this resource the biggest in Europe, researchers will have access to a huge amount of information about the part that environment and genetics play in disease.

'The genetics work done by this group will be incorporated into UK Biobank for other researchers working in different areas to use in their own studies, bringing closer the promise of new treatments and drugs for a whole range of diseases and conditions.'

The team now hopes to expands its research into the remainder of the 500,000 participants once the data becomes available in 2016.

Meanwhile researchers in Japan have identified a treatable genetic mutation in 75 percent of a group of young lung cancer patients that can cause normal cells to become cancerous.