2022
DOI: 10.1080/17476348.2022.2145948
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Idiopathic pulmonary fibrosis and lung cancer: targeting the complexity of the pharmacological interconnection

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Cited by 4 publications
(1 citation statement)
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“…In experimental studies with mice, PD-L1 expression was noted to be higher in injury-activated alveolar epithelial cells and in human donor samples with end-stage IPF [58 ▪ ], suggesting that disinhibition of immune cells might exacerbate this injured tissue. Though IPF and lung cancer are not often thought to share common genetic pathways, several genes that drive inflammation and fibrosis in IPF are also overexpressed in lung cancer, including TGF-β1, IL-1 receptor alpha, IL-4, IL-8, and others [59,60 ▪ ]. The shared genetic landscape of IPF and NSCLC has led to the use of antifibrotics to treat NSCLC, though evidence of efficacy is yet lacking [61,62 ▪ ].…”
Section: Preexisting Interstitial Lung Diseasementioning
confidence: 99%
“…In experimental studies with mice, PD-L1 expression was noted to be higher in injury-activated alveolar epithelial cells and in human donor samples with end-stage IPF [58 ▪ ], suggesting that disinhibition of immune cells might exacerbate this injured tissue. Though IPF and lung cancer are not often thought to share common genetic pathways, several genes that drive inflammation and fibrosis in IPF are also overexpressed in lung cancer, including TGF-β1, IL-1 receptor alpha, IL-4, IL-8, and others [59,60 ▪ ]. The shared genetic landscape of IPF and NSCLC has led to the use of antifibrotics to treat NSCLC, though evidence of efficacy is yet lacking [61,62 ▪ ].…”
Section: Preexisting Interstitial Lung Diseasementioning
confidence: 99%