American Association for Cancer Research
mcr-23-0480_supplemental_figure_s2_suppsf2.pdf (502.46 kB)

Supplemental Figure S2 from Modeling Molecular Pathogenesis of Idiopathic Pulmonary Fibrosis-Associated Lung Cancer in Mice

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posted on 2024-03-01, 13:00 authored by Ivana Barravecchia, Jennifer M. Lee, Jason Manassa, Brian Magnuson, Sarah F. Ferris, Sophia Cavanaugh, Nina G. Steele, Carlos E. Espinoza, Craig J. Galban, Nithya Ramnath, Timothy L. Frankel, Marina Pasca di Magliano, Stefanie Galban

Supplemental Figure S2. Expression of immune cell surface markers by CyTOF.


Rogel Cancer Center, University of Michigan (Rogel Cancer Center)

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)

United States Department of Health and Human Services

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National Cancer Institute (NCI)

United States Department of Health and Human Services

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Idiopathic pulmonary fibrosis (IPF) is characterized by progressive, often fatal loss of lung function due to overactive collagen production and tissue scarring. Patients with IPF have a sevenfold-increased risk of developing lung cancer. The COVID-19 pandemic has increased the number of patients with lung diseases, and infection can worsen prognoses for those with chronic lung diseases and disease-associated cancer. Understanding the molecular pathogenesis of IPF-associated lung cancer is imperative for identifying diagnostic biomarkers and targeted therapies that will facilitate prevention of IPF and progression to lung cancer. To understand how IPF-associated fibroblast activation, matrix remodeling, epithelial-to-mesenchymal transition (EMT), and immune modulation influences lung cancer predisposition, we developed a mouse model to recapitulate the molecular pathogenesis of pulmonary fibrosis–associated lung cancer using the bleomycin and Lewis lung carcinoma models. We demonstrate that development of pulmonary fibrosis–associated lung cancer is likely linked to increased abundance of tumor-associated macrophages and a unique gene signature that supports an immune-suppressive microenvironment through secreted factors. Not surprisingly, preexisting fibrosis provides a pre-metastatic niche and results in augmented tumor growth, and tumors associated with bleomycin-induced fibrosis are characterized by a dramatic loss of cytokeratin expression, indicative of EMT. This characterization of tumors associated with lung diseases provides new therapeutic targets that may aid in the development of treatment paradigms for lung cancer patients with preexisting pulmonary diseases.

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