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Articles by Robert Homer
Editorial Expression of Concern: Thyroid hormone inhibits lung fibrosis in mice by improving epithelial mitochondrial function
Addendum to: Nature Medicine https://doi.org/10.1038/nm.4447, published online 4 December 2017. The Editors would like to alert the readers that concerns have been raised regarding some of the data presented in the figures, specifically: In Fig. 3n (and the associated uncropped gel images in Fig. S4c and d), the AECIIS PINK1 and MLE-12 PGC-1α blots appear highly similar; In Fig. 4a (and the associated uncropped gel images in Fig.
Author Correction: Uncovering the role of LINE-1 in the evolution of lung adenocarcinoma
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Correction to: Nature https://doi.org/10.1038/s41586-025-09825-y Published online 10 December 2025 It has been drawn to our attention that some statements in the initially published version of this article could be interpreted as supporting a direct mechanistic role for ZNF695 in L1 regulation. As there was no experimental evidence for such a role, the article has been corrected.
By Tongwu Zhang, Wei Zhao, Christopher Wirth, Marcos Díaz-Gay, Jinhu Yin, Monia Cecati, Francesca Marchegiani, Phuc H. Hoang, Charles A. LeDuc, Marina K Baine, William Travis, Lynette M. Sholl, Philippe Joubert, Jian Sang, Michelle Antony, Alyssa Klein, Azhar Khandekar, Caleb Hartman, Jennifer Rosenbaum, Monjoy Saha, Olivia Lee, Kristine Jones, Neil E Caporaso, Chao Agnes Hsiung, Chih-Yi Chen, Eric S. Edell, Jacobo Santamaria, Matthew B Schabath, Sai Yendamuri, Marta Manczuk, Jolanta Lissowska, Oxana Shangina, David Zaridze, Ivana Holcatova, Dana Mates, Saša Milosavljević, Milan Savic, Yohan Bossé, David C. Christiani, Valerie Gaborieau, Paul Brennan Verified, Geoffrey Liu, Paul Hofman, Robert Homer, Soo-Ryum Yang, Angela C. Pesatori, Dario Consonni, Lixing Yang, Bin Zhu, Jianxin Shi, Kevin Brown, Nathaniel Rothman, Stephen J. Chanock, Ludmil B. Alexandrov, Jiyeon Choi, Maurizio Cardelli, Qing Lan, Martin Nowak, David C. Wedge, Maria Landi, John P. McElderry, Frank J. Colón-Matos, Mona Miraftab, Kin Chung Leung, Anush Mukeria, Bonnie E. Gould Rothberg
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Nature
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Aberrant cellular communities underlying disease heterogeneity in chronic obstructive pulmonary disease - Nature Genetics
Abstract Chronic obstructive pulmonary disease (COPD) is clinically and molecularly heterogeneous. To investigate COPD heterogeneity, we profiled lung tissue by single-nucleus RNA sequencing from 141 study participants (1,516,727 nuclei) and identified shifts in cell composition and emergent cell states that correlated with lung function, emphysema and composite symptom scores.
Microbiome analysis of 940 lung cancers in never-smokers reveals lack of clinically relevant associations - Nature Communications
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Abstract In spite of the growing interest in the microbiome in human cancer, there are currently only small-scale lung cancer microbiome studies conducted directly on tissue. As part of the Sherlock-Lung study, we studied the microbiomes of 940 lung cancers (4090 samples) in never smokers (LCINS) directly from lung tissue using three data types: 16S rRNA gene sequencing (16S), whole-genome sequencing (WGS) with paired blood, and RNA-seq.
By Tongwu Zhang, Wei Zhao, Phuc H. Hoang, Caleb Hartman, Monjoy Saha, Olivia Lee, Kristine Jones, Bin Zhu, Marcos Díaz-Gay, Matthew B Schabath, Marta Manczuk, Jolanta Lissowska, Ivana Holcatova, Yohan Bossé, David C. Christiani, Paul Hofman, Lynette M. Sholl, Robert Homer, Qing Lan, David C. Wedge, Ludmil B. Alexandrov, Stephen J. Chanock, Emily Vogtmann, Christian C Abnet, Jianxin Shi
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Nature
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Uncovering the role of LINE-1 in the evolution of lung adenocarcinoma - Nature
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Abstract Understanding lung cancer evolution can identify tools for intercepting its growth1,2. Here, in a landscape analysis of 1,024 lung adenocarcinomas (LUADs) with deep whole-genome sequencing integrated with multiomic data, we identified 542 LUADs with a diverse clonal architecture. In this group, we observed divergent evolutionary trajectories based on tobacco smoking exposure, ancestry and sex.
By Tongwu Zhang, Wei Zhao, Christopher Wirth, Marcos Díaz-Gay, Jinhu Yin, Phuc H. Hoang, Lynette M. Sholl, Monjoy Saha, Olivia Lee, Kristine Jones, Jacobo Santamaria, Matthew B Schabath, Marta Manczuk, Jolanta Lissowska, Yohan Bossé, David C. Christiani, Paul Hofman, Robert Homer, Angela C. Pesatori, Dario Consonni, Bin Zhu, Jianxin Shi, Stephen J. Chanock, Ludmil B. Alexandrov, Jiyeon Choi, Maurizio Cardelli, Qing Lan, David C. Wedge
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Nature
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The mutagenic forces shaping the genomes of lung cancer in never smokers - Nature
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Abstract Lung cancer in never smokers (LCINS) accounts for around 25% of all lung cancers1,2 and has been associated with exposure to second-hand tobacco smoke and air pollution in observational studies3,4,5. Here we use data from the Sherlock-Lung study to evaluate mutagenic exposures in LCINS by examining the cancer genomes of 871 treatment-naive individuals with lung cancer who had never smoked, from 28 geographical locations.
By Marcos Díaz-Gay, Tongwu Zhang, Phuc H. Hoang, Lynette M. Sholl, Wei Zhao, Shuvro P Nandi, Raviteja Vangara, Oriol Pich, Charles Swanton, Olivia Lee, Kristine Jones, Pilar Gallego-García, Jacobo Santamaria, Matthew B Schabath, Marta Manczuk, Jolanta Lissowska, Yohan Bossé, David C. Christiani, Paul Hofman, Jianxin Shi, David C. Wedge, Robert Homer, Angela C. Pesatori, Dario Consonni, Qing Lan, Bin Zhu, Stephen J. Chanock, Jiyeon Choi, Ludmil B. Alexandrov, Caleb Hartman
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Nature
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APOBEC affects tumor evolution and age at onset of lung cancer in smokers - Nature Communications
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Abstract Most solid tumors harbor somatic mutations attributed to off-target activities of APOBEC3A (A3A) and/or APOBEC3B (A3B). However, how APOBEC3A/B enzymes affect tumor evolution in the presence of exogenous mutagenic processes is largely unknown. Here, multi-omics profiling of 309 lung cancers from smokers identifies two subtypes defined by low (LAS) and high (HAS) APOBEC mutagenesis.
By Tongwu Zhang, Phuc H. Hoang, Wei Zhao, Leszek J. Klimczak, Alyssa Klein, Christopher Wirth, Marcos Díaz-Gay, Raviteja Vangara, Scott Lawrence, Bin Zhu, Teresa M. Przytycka, Jianxin Shi, Robert Homer, Dario Consonni, Stephen J. Chanock, David C. Wedge, Dmitry Gordenin, Ludmil B. Alexandrov, Reuben S. Harris, Angela C. Pesatori
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Nature
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Secretory leukocyte protease inhibitor influences periarticular joint inflammation in Borrelia burgdorferi-infected mice
eLife Assessment This study presents a valuable finding on the role of secretory leukocyte protease inhibitors (SLPIs) in developing Lyme disease in mice infected with Borrelia burgdorferi. The evidence supporting the authors' claims is solid. However, several concerns raised by the reviewers remain unaddressed. This paper would be of interest to scientists in the infectious inflammatory disease field.
Secretory leukocyte protease inhibitor influences periarticular joint inflammation in B. burgdorferi-infected mice
Abstract Lyme disease, caused by Borrelia burgdorferi, is the most common tick-borne infection in the United States. Arthritis is a major clinical manifestation of infection, and synovial tissue damage has been attributed to the excessive pro-inflammatory responses. The secretory leukocyte protease inhibitor (SLPI) promotes tissue repair and exerts anti-inflammatory effects. The role of SLPI in the development of Lyme arthritis in C57BL/6 mice, which can be infected with B.
SRC and TKS5 mediated podosome formation in fibroblasts promotes extracellular matrix invasion and pulmonary fibrosis - Nature Communications
Abstract The activation and accumulation of lung fibroblasts resulting in aberrant deposition of extracellular matrix components, is a pathogenic hallmark of Idiopathic Pulmonary Fibrosis, a lethal and incurable disease. In this report, increased expression of TKS5, a scaffold protein essential for the formation of podosomes, was detected in the lung tissue of Idiopathic Pulmonary Fibrosis patients and bleomycin-treated mice.
Inhibition of type 1 immunity with tofacitinib is associated with marked improvement in longstanding sarcoidosis - Nature Communications
Abstract Sarcoidosis is an idiopathic inflammatory disorder that is commonly treated with glucocorticoids. An imprecise understanding of the immunologic changes underlying sarcoidosis has limited therapeutic progress. Here in this open-label trial (NCT03910543), 10 patients with cutaneous sarcoidosis are treated with tofacitinib, a Janus kinase inhibitor.
A rare presentation of pulmonary sarcoidosis as a solitary lung mass: a case report
Atypical radiographic presentations of pulmonary sarcoidosis occur in 15–25% of patients [3]. These findings can include diffuse ground-glass opacities, honeycombing, multiple nodules, or necrotizing consolidations [3]. A large, solitary lung mass, as described in our patient’s case, has rarely been reported, and its incidence is unknown; it is likely to be the result of individual granulomas that have coalesced to produce the appearance of a mass [5].
Diagnosing idiopathic pulmonary fibrosis without a lung biopsy: honeycombing not required
Nearly 50?years ago, idiopathic interstitial pneumonias (IIPs) were defined by Liebow and Carrington based on the histological pattern present in the lung.1 ,2 Today, we consider histological patterns in the context of clinical and radiological information in order to diagnose a specific IIP, a paradigm shift initially introduced by a Consensus Statement published by the American Thoracic Society and European Respiratory Society in 2002 and developed further in 2011.3 With regard to...
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