Paired analysis of tumor mutation burden for lung adenocarcinoma and associated idiopathic pulmonary fibrosis

Yasuto Yoneshima, Eiji Iwama, Shingo Matsumoto, Taichi Matsubara, Testuzo Tagawa, Keiichi Ota, Kentaro Tanaka, Mitsuhiro Takenoyama, Tatsuro Okamoto, Koichi Goto, Masaki Mori, Isamu Okamoto

研究成果: Contribution to journalArticle査読

1 被引用数 (Scopus)

抄録

Genetic alterations underlying the development of lung cancer in individuals with idiopathic pulmonary fibrosis (IPF) have remained unclear. To explore whether genetic alterations in IPF tissue contribute to the development of IPF-associated lung cancer, we here evaluated tumor mutation burden (TMB) and somatic variants in 14 paired IPF and tumor samples from patients with IPF-associated lung adenocarcinoma. We also determined TMB for 22 samples of lung adenocarcinoma from patients without IPF. TMB for IPF-associated lung adenocarcinoma was significantly higher than that for matched IPF tissue (median of 2.94 vs. 1.26 mutations/Mb, P = 0.002). Three and 102 somatic variants were detected in IPF and matched lung adenocarcinoma samples, respectively, with only one pair of specimens sharing one somatic variant. TMB for IPF-associated lung adenocarcinoma was similar to that for lung adenocarcinoma samples with driver mutations (median of 2.94 vs. 2.51 mutations/Mb) and lower than that for lung adenocarcinoma samples without known driver mutations (median of 2.94 vs. 5.03 mutations/Mb, P = 0.130) from patients without IPF. Our findings suggest that not only the accumulation of somatic mutations but other factors such as inflammation and oxidative stress might contribute to the development and progression of lung cancer in patients with IPF.

本文言語英語
論文番号12732
ジャーナルScientific reports
11
1
DOI
出版ステータス出版済み - 12 2021

All Science Journal Classification (ASJC) codes

  • 一般

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