MedWire News: A history of pulmonary tuberculosis (TB) is associated with a higher incidence of mutations in the epidermal growth factor receptor gene (EGFR) in patients with adenocarcinoma of the lung, researchers report in the Journal of Thoracic Oncology.
It has been suggested that pulmonary TB increases a person's risk for lung cancer via pulmonary inflammation and fibrosis that may induce genetic damage, leading to carcinogenesis of the pulmonary parenchymal tissue, explain Yuh-Min Chen (Taipei Veterans Hospital, Taiwan, China) and colleagues.
However, the pathogenic linkage between pulmonary TB and lung cancer is still unclear.
In the present study, Chen and team investigated the association between mutations in the EGFR gene, which have been well documented in lung cancer patients, and pulmonary TB.
They retrospectively reviewed the medical records of 275 patients (48% men) who had pulmonary adenocarcinoma of the lungs and a documented tumor EGFR mutation status.
Among the patients, 17 (6.2%) had a clinical history of pulmonary TB infection and 72 (26.2%) had old TB lesions on chest computed tomography scans. There were 14 (5.1%) patients with scar cancer (cancer that had merged with TB fibrotic scars or granuloma lesions) and 191 (69.5%) with an EGFR mutation, including 118 exon 19 deletions, 59 exon 21 L858R point mutations, eight exon 18 mutations, and 10 exon 20 mutations.
The researchers found that patients with old TB lesions had a significantly higher incidence of EGFR mutations than those without, at 80.6% versus 65.5%. All patients with scar cancer had an EGFR mutation, compared with 67.8% of patients who did not have scar cancer.
When looking at specific mutations, Chen and team observed significantly more exon 19 deletions in patients with old TB lesions than in those without (68.1 vs 34.0%), and in patients with scar cancer than in those without (92.9 vs 40.2%).
Therefore, "old TB lesions and scar cancer had a statistically significant association with EGFR mutation, especially exon 19 deletions," say the researchers.
Indeed, multivariate analysis showed that patients with old TB lesions and those with scar cancer were four times and 19 times more likely to have exon 19 deletions, respectively, than patients without each of these features.
By contrast, exon 21 L858R mutations were less common in patients with old TB lesions than in those without, at 8.3% versus 26.1%.
Chen et al say their results indicate that "the scarring process of old TB lesions may play an important role in the formation of lung cancer."
In addition, "the inflammatory process of pulmonary TB may lead to cellular exon 19 deletions but not exon 21 L858R mutations."
These suggestions were substantiated by the fact that the proportion of tumor EGFR mutations, especially exon 19 deletions, was higher when the location of the lung cancer was closer to the old TB lesions.
The researchers conclude that a relationship exists "between pulmonary TB and EGFR mutations in patients with adenocarcinoma of the lungs."
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