表皮生長(zhǎng)因子受體蛋白結(jié)構(gòu)圖,，圖片來(lái)自維基共享資源,。
人們長(zhǎng)期就懷疑肺結(jié)核病(tuberculosis)會(huì)增加一個(gè)人患肺癌的風(fēng)險(xiǎn),，因?yàn)榉尾垦装Y和纖維化能夠誘導(dǎo)基因損傷,。然而,，特異性基因變化和疾病的直接證據(jù)一直沒(méi)有廣泛地報(bào)道過(guò),。
發(fā)表在國(guó)際肺癌協(xié)會(huì)2012年2月那期Journal of Thoracic Oncology雜志上的研究表明肺結(jié)核病與表皮生長(zhǎng)因子受體(epidermal growth factor receptor, EGFR)---一種在非小細(xì)胞肺癌(non-small cell lung cancer)中發(fā)現(xiàn)的基因突變類型---突變存在關(guān)聯(lián),。研究人員下結(jié)論道，在肺腺癌(lung adenocarcinoma)病人中肺結(jié)核病和EGFR突變存在關(guān)聯(lián),。腺癌是最為常見(jiàn)的肺癌,。
研究人員在1999年6月到2011年1月期間研究了275名病人。在這些病人當(dāng)中,，191名發(fā)生EGFR突變,。他們的發(fā)現(xiàn)表明“舊有的肺結(jié)核病和瘢痕癌(scar cancer，譯者注：臨床上一種特殊類型的肺癌與肺結(jié)核有關(guān),，多為肺腺癌)跟EGFR突變,，特別是第19個(gè)外顯子缺失，存在統(tǒng)計(jì)學(xué)上顯著性的關(guān)聯(lián)”,，其中這個(gè)外顯子缺失是最為常見(jiàn)的腫瘤EGFR突變形式,。
在東亞地區(qū)，比如中國(guó)臺(tái)灣,，人們發(fā)現(xiàn)較高的腫瘤EGFR突變發(fā)生率(incidence),，就像肺結(jié)核菌感染的盛行率(prevalence)一樣。好消息是發(fā)生EGFR突變的腫瘤當(dāng)用EGFR-酪氨酸激酶抑制物治療時(shí)有75%的反應(yīng)率(response rate),。根據(jù)該項(xiàng)研究,，這可能是為什么“(當(dāng)進(jìn)行藥物治療后)那些遭受舊有肺結(jié)核病損傷的病人若發(fā)生EGFR突變或者說(shuō)它的外顯子發(fā)生突變要比那些沒(méi)有發(fā)生突變的病人存活更長(zhǎng)時(shí)間”。(生物谷：towersimper編譯)
doi:10.1097/JTO.0b013e31823c588d
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PMID:
Association between Tumor Epidermal Growth Factor Receptor Mutation and Pulmonary Tuberculosis in Patients with Adenocarcinoma of the Lungs
Luo, Yung-Hung; Wu, Chieh-Hung; Wu, Wen-Shuo; Huang, Chu-Yun; Su, Wei-Juin; Tsai, Chun-Ming; Lee, Yu-Chin; Perng, Reury-Perng; Chen, Yuh-Min
Background: The possible association between pulmonary tuberculosis (TB) and lung cancer development has been studied for several decades. However, the association between epidermal growth factor receptor (EGFR) mutation status and pulmonary TB in patients with adenocarcinoma of the lungs is unknown.
Methods: We reviewed the data of our patients with adenocarcinoma of the lungs who had a clinical history of pulmonary TB or old TB lesions shown on chest computed tomography scan and evaluated the association between tumor EGFR mutation status and pulmonary TB.
Results: From June 1999 to January 2011, there were 275 patients with pulmonary adenocarcinoma with tumor EGFR mutation data available for analysis. Of them, 191 patients had EGFR mutations, 17 had a clinical history of pulmonary TB infection, 72 had old TB lesions on chest computed tomography scans, and 14 had scar cancer. Patients with old TB lesions had a higher incidence of EGFR mutation than those without (p = 0.018). Exon 19 deletions occurred more frequently in patients with old TB lesions than in patients without (p < 0.001). Those patients with old TB lesions who had EGFR mutations or exon 19 mutations survived longer than those who did not (p = 0.014 and 0.001, respectively). Patients with exon 19 deletions and old TB lesions showed no survival difference compared with those with exon 19 deletions and without old TB lesions (p = 0.271).
Conclusions: Patients with pulmonary adenocarcinoma who had scar cancer or had old TB lesions had a higher probability of having EGFR mutations, especially exon 19 deletions.
