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

Abstract 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 bur...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Yasuto Yoneshima, Eiji Iwama, Shingo Matsumoto, Taichi Matsubara, Testuzo Tagawa, Keiichi Ota, Kentaro Tanaka, Mitsuhiro Takenoyama, Tatsuro Okamoto, Koichi Goto, Masaki Mori, Isamu Okamoto
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/9cdaf15acea343ac89678c3375dbc507
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:9cdaf15acea343ac89678c3375dbc507
record_format	dspace
spelling	oai:doaj.org-article:9cdaf15acea343ac89678c3375dbc5072021-12-02T17:41:29ZPaired analysis of tumor mutation burden for lung adenocarcinoma and associated idiopathic pulmonary fibrosis10.1038/s41598-021-92098-y2045-2322https://doaj.org/article/9cdaf15acea343ac89678c3375dbc5072021-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-92098-yhttps://doaj.org/toc/2045-2322Abstract 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.Yasuto YoneshimaEiji IwamaShingo MatsumotoTaichi MatsubaraTestuzo TagawaKeiichi OtaKentaro TanakaMitsuhiro TakenoyamaTatsuro OkamotoKoichi GotoMasaki MoriIsamu OkamotoNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-7 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Yasuto Yoneshima Eiji Iwama Shingo Matsumoto Taichi Matsubara Testuzo Tagawa Keiichi Ota Kentaro Tanaka Mitsuhiro Takenoyama Tatsuro Okamoto Koichi Goto Masaki Mori Isamu Okamoto Paired analysis of tumor mutation burden for lung adenocarcinoma and associated idiopathic pulmonary fibrosis
description	Abstract 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.
format	article
author	Yasuto Yoneshima Eiji Iwama Shingo Matsumoto Taichi Matsubara Testuzo Tagawa Keiichi Ota Kentaro Tanaka Mitsuhiro Takenoyama Tatsuro Okamoto Koichi Goto Masaki Mori Isamu Okamoto
author_facet	Yasuto Yoneshima Eiji Iwama Shingo Matsumoto Taichi Matsubara Testuzo Tagawa Keiichi Ota Kentaro Tanaka Mitsuhiro Takenoyama Tatsuro Okamoto Koichi Goto Masaki Mori Isamu Okamoto
author_sort	Yasuto Yoneshima
title	Paired analysis of tumor mutation burden for lung adenocarcinoma and associated idiopathic pulmonary fibrosis
title_short	Paired analysis of tumor mutation burden for lung adenocarcinoma and associated idiopathic pulmonary fibrosis
title_full	Paired analysis of tumor mutation burden for lung adenocarcinoma and associated idiopathic pulmonary fibrosis
title_fullStr	Paired analysis of tumor mutation burden for lung adenocarcinoma and associated idiopathic pulmonary fibrosis
title_full_unstemmed	Paired analysis of tumor mutation burden for lung adenocarcinoma and associated idiopathic pulmonary fibrosis
title_sort	paired analysis of tumor mutation burden for lung adenocarcinoma and associated idiopathic pulmonary fibrosis
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/9cdaf15acea343ac89678c3375dbc507
work_keys_str_mv	AT yasutoyoneshima pairedanalysisoftumormutationburdenforlungadenocarcinomaandassociatedidiopathicpulmonaryfibrosis AT eijiiwama pairedanalysisoftumormutationburdenforlungadenocarcinomaandassociatedidiopathicpulmonaryfibrosis AT shingomatsumoto pairedanalysisoftumormutationburdenforlungadenocarcinomaandassociatedidiopathicpulmonaryfibrosis AT taichimatsubara pairedanalysisoftumormutationburdenforlungadenocarcinomaandassociatedidiopathicpulmonaryfibrosis AT testuzotagawa pairedanalysisoftumormutationburdenforlungadenocarcinomaandassociatedidiopathicpulmonaryfibrosis AT keiichiota pairedanalysisoftumormutationburdenforlungadenocarcinomaandassociatedidiopathicpulmonaryfibrosis AT kentarotanaka pairedanalysisoftumormutationburdenforlungadenocarcinomaandassociatedidiopathicpulmonaryfibrosis AT mitsuhirotakenoyama pairedanalysisoftumormutationburdenforlungadenocarcinomaandassociatedidiopathicpulmonaryfibrosis AT tatsurookamoto pairedanalysisoftumormutationburdenforlungadenocarcinomaandassociatedidiopathicpulmonaryfibrosis AT koichigoto pairedanalysisoftumormutationburdenforlungadenocarcinomaandassociatedidiopathicpulmonaryfibrosis AT masakimori pairedanalysisoftumormutationburdenforlungadenocarcinomaandassociatedidiopathicpulmonaryfibrosis AT isamuokamoto pairedanalysisoftumormutationburdenforlungadenocarcinomaandassociatedidiopathicpulmonaryfibrosis
_version_	1718379661050773504

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

Ejemplares similares