Gene mutation linked TB with pulmonary adenocarcinoma
Luo YH. J Thorac Oncol. 2012;7:299-305.
Patients with pulmonary adenocarcinoma who had scar cancer or aged pulmonary tuberculosis lesions exhibited a higher probability of having epidermal growth factor receptor mutations, especially exon 19 deletions, according to study findings published in the Journal of Thoracic Oncology.
To evaluate the association between tumor EGFR mutations and pulmonary tuberculosis (TB), researchers from the Taipei Veterans General Hospital in Taiwan retrospectively reviewed the chart records of patients with pulmonary adenocarcinoma who had received diagnosis, staging and treatment.
Patients included in the study had either been diagnosed with pulmonary TB or had chest CT images compatible with previous TB infection. After determining the existence and location of pulmonary TB lesions, chest CT scans were evaluated for fibrotic change, fibronodular lesions, pleural thickening, calcified nodules, scars, the location of the primary tumor, and TB lesions in the same or different lobe of the primary lesion of lung cancer. In addition, EGFR mutation analysis was performed with nucleotide sequence analysis, in which tumor EGFR mutations were defined as those with exons 18 to 21 mutations.
From June 1999 to January 2011, 275 patients with pulmonary adenocarcinoma with tumor EGFR mutation data were enrolled in the study for analysis. Among these patients, 191 patients exhibited EGFR mutations, 72 had aged TB lesions on chest CT scans, 17 had a clinical history of pulmonary TB infection and 14 had scar cancer.
According to study results, patients with aged TB lesions expressed a higher incidence of EGFR mutation than those without (P=.018). Exon 19 deletions occurred more frequently in patients with aged TB lesions than in patients without (P<.001). Those patients with aged TB lesions who had EGFR mutations or exon 19 mutations survived longer than those who did not. Patients with exon 19 deletions and aged TB lesions showed no survival difference compared with those with exon 19 deletions and without old TB lesions (P=.271).
“The pathogenic linkage between pulmonary TB and lung cancer is still unclear,” the researchers said. “A chronic inflammatory process because of latent TB infection may serve as a cause of lung carcinogenesis and results in remodeling of lung tissue, activation of an atypical differentiation pathway, and finally malignant transformation.”
Disclosure: The researchers report no relevant financial disclosures.
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