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  • The development could one day lead to life-saving early detection of squamous cell lung cancer, which accounts for up to 30 per cent of all lung cancers.

    There is still years of work ahead before the discovery could be used to help patients, with ex-smokers those most likely to benefit.

    The breakthrough was made by researchers at the Walter and Eliza Hall Institute in Melbourne, led by PhD student Clare Weeden and Dr Marie-Liesse Asselin-Labat.

    Using donated human tissue, they looked at the cells in the airway of the lung, called basal stem cells, and noticed that when exposed to harmful chemicals like cigarette smoke they would rapidly repair the damage.

    But there was a problem with how they were doing that. The rapid repair process was prone to errors. And these rapid repair basal stem cells were far more active in the lungs of smokers and ex-smokers.

    “It was like this lightbulb went off,” Ms Weeden said.

    “I went back to the biobank and asked for the smoking history of all the patient samples we had received and stayed in all weekend and furiously put all this data together.

    “At the end of it I found this really striking result that if you were a heavy smoker then you had really activated basal stem cells, and if you never smoked cigarettes they hardly grew at all.”

    Then genetic analysis using a technique developed by the institute’s bioinformatics department confirmed a link between the genetic signatures of the lung-based basal stem cells and the cancer.

    “We think these cells are the ‘cell of origin’ or the first cells that acquire genetic mutations that lead to the onset of this cancer forming,” Ms Weeden said.

    “The hope going forward is that our work will be a gateway to new, tailored prevention and treatment measures for patients with lung diseases.”

    The potential ability to intervene might be useful for ex-smokers but would not be a free pass to keep smoking.

    “If a drug is able to turn off the function of the basal stem cell yet the lung continues to be damaged through smoking, there is a risk of other lung problems occurring as the body’s natural repair mechanism is missing,” Ms Weeden said.

    “There are also other forms of lung cancer caused by smoking that do not arise from basal stem cells.”

    Professor Sanchia Aranda, the chief executive of Cancer Council Australia, said that although the research had a long way to go, it showed promise, particularly for early detection.

    “The holy grail of lung cancer treatment is the ability to find early diagnostic capability,” she said.

    “We very much want to see this kind of research and its logical therapeutic pathways developed because it’s still almost a universally fatal disease.”

    The finding were published in PLOS Biology.


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