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Mutations in the LKBI tumour suppressor gene linked to non-small cell lung cancer in Caucasians
  1. R Curley
  1. Dr R Curley, The Royal Hallamshire Hospital, Sheffield, UK; rachaelcurley1{at}hotmail.com

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Lung cancer remains the most common cause of cancer-related death in the UK. However, patients with non-small cell lung cancer (NSCLC) may benefit from surgery or radiotherapy, providing a cure in a small proportion. Mutations in the LKBI tumour suppressor gene have been found in several human cancers including NSCLC. This study explores the incidence of LKBI mutations in patients with NSCLC, the frequency in different ethnic groups and associations with other clinicopathological characteristics (sex, smoking, tumour stage, histology and outcome).

Tumour tissue collected from 310 patients at curative surgical resections was screened for LKBI mutations. These were present in 11% of the tumours, which was more than other common solid malignancies (0–4%). Mutations were more prevalent in the Caucasian group (17%) than the Asian group (5%), with an association between smoking (>10 pack-years) and the presence of mutations. Despite this, the study fails to address fully the fact that smokers were predominantly Caucasian, confounding the ethnic divide. Surprisingly, LKBI mutations were more common in adenocarcinomas (13%) as, histologically, this is the most frequent lung cancer in non-smokers. Statistically, LKBI mutation status was not found to affect outcomes in patients with stage I and II NSCLC treated with surgery alone, although the study showed shorter survival rates.

The complexity of this study and numerous influencing factors highlight the multifactorial aetiology of NSCLC and an important genetic link, raising the question whether genetic screening in the future could help detect those at risk of developing a potentially curable cancer.

▸ Koivunen JP, Kim J, Lee J, et al. Mutations in the LKBI tumour suppressor are frequently detected in tumours from Caucasian but not Asian lung cancer patients. Br J Cancer 2008;99:245–52.

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