Robert J. Homer mainly focuses on Immunology, Inflammation, Interleukin 13, Lung and Cytokine. The study incorporates disciplines such as Fibrosis and Pulmonary fibrosis in addition to Immunology. His Pulmonary fibrosis study combines topics from a wide range of disciplines, such as CXCL10 and Eotaxin.
His Inflammation research includes elements of Eosinophil, Transgene, Eosinophilia, Matrix metalloproteinase and Macrophage. His Interleukin 13 research is multidisciplinary, incorporating perspectives in Effector and Chitinase. Robert J. Homer works mostly in the field of Lung, limiting it down to topics relating to Pathology and, in certain cases, CD8, Antibody and Pulmonary edema, as a part of the same area of interest.
His primary scientific interests are in Immunology, Inflammation, Pathology, Lung and Cancer research. The Immunology study which covers Fibrosis that intersects with Transforming growth factor beta. His biological study spans a wide range of topics, including Receptor, Matrix metalloproteinase, Transgene and Cell biology.
His research in Pathology intersects with topics in Respiratory disease and Interstitial lung disease. His Lung study deals with Airway intersecting with Asthma. In his study, Adenocarcinoma is inextricably linked to Lung cancer, which falls within the broad field of Cancer research.
Robert J. Homer focuses on Pathology, Cancer research, Lung, Lung cancer and Idiopathic pulmonary fibrosis. His work deals with themes such as Internal medicine and Antibody, which intersect with Pathology. The concepts of his Cancer research study are interwoven with issues in Epidermal growth factor receptor, Adrenergic, Osimertinib and Transcription factor.
His Lung research incorporates themes from Inflammation, Immunology, Anatomy & histology and Parenchyma. His Acetylcholine receptor research extends to Immunology, which is thematically connected. His studies in Idiopathic pulmonary fibrosis integrate themes in fields like Fibrosis, Pulmonary fibrosis, Myofibroblast and Fibroblast.
Idiopathic pulmonary fibrosis, Pathology, Lung, Cancer research and Virus are his primary areas of study. The Idiopathic pulmonary fibrosis study combines topics in areas such as Pulmonary fibrosis and Interstitial lung disease. While the research belongs to areas of Pulmonary fibrosis, he spends his time largely on the problem of In vivo, intersecting his research to questions surrounding Matrix metalloproteinase, Inflammation, CD68 and Interleukin 13.
Many of his research projects under Pathology are closely connected to Intraclass correlation with Intraclass correlation, tying the diverse disciplines of science together. The various areas that Robert J. Homer examines in his Cancer research study include Cancer, Plexin, DNA methylation, Transcription factor and Fibrosis. His Mucociliary clearance study frequently draws connections to adjacent fields such as Immunology.
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Pulmonary expression of interleukin-13 causes inflammation, mucus hypersecretion, subepithelial fibrosis, physiologic abnormalities, and eotaxin production
Zhou Zhu;Robert J. Homer;Robert J. Homer;Zhonde Wang;Qingsheng Chen.
Journal of Clinical Investigation (1999)
Regulation of lung injury and repair by Toll-like receptors and hyaluronan.
Dianhua Jiang;Jiurong Liang;Juan Fan;Shuang Yu.
Nature Medicine (2005)
Interleukin-13 Induces Tissue Fibrosis by Selectively Stimulating and Activating Transforming Growth Factor β1
Chun Geun Lee;Robert J. Homer;Zhou Zhu;Sophie Lanone.
Journal of Experimental Medicine (2001)
Acidic Mammalian Chitinase in Asthmatic Th2 Inflammation and IL-13 Pathway Activation
Zhou Zhu;Tao Zheng;Robert J. Homer;Yoon Keun Kim.
Airway remodeling in asthma.
Jack A. Elias;Zhou Zhu;Geoffrey Chupp;Robert J. Homer.
Journal of Clinical Investigation (1999)
Inducible targeting of IL-13 to the adult lung causes matrix metalloproteinase– and cathepsin-dependent emphysema
Tao Zheng;Zhou Zhu;Zhongde Wang;Robert J. Homer;Robert J. Homer.
Journal of Clinical Investigation (2000)
A SNP in a let-7 microRNA Complementary Site in the KRAS 3′ Untranslated Region Increases Non–Small Cell Lung Cancer Risk
Lena J. Chin;Elena Ratner;Shuguang Leng;Rihong Zhai.
Cancer Research (2008)
Vascular endothelial growth factor (VEGF) induces remodeling and enhances TH2-mediated sensitization and inflammation in the lung.
Chun Geun Lee;Holger Link;Peter Baluk;Robert J Homer.
Nature Medicine (2004)
Induction of Airway Mucus Production By T Helper 2 (Th2) Cells: A Critical Role For Interleukin 4 In Cell Recruitment But Not Mucus Production
Lauren Cohn;Robert J. Homer;Anthony Marinov;John Rankin.
Journal of Experimental Medicine (1997)
A prospective, multi-institutional, pathologist-based assessment of 4 immunohistochemistry assays for PD-L1 expression in non–small cell lung cancer
David L. Rimm;Gang Han;Janis M. Taube;Eunhee S. Yi.
JAMA Oncology (2017)
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