M
Michael Detmar
Researcher at École Polytechnique Fédérale de Lausanne
Publications - 351
Citations - 43193
Michael Detmar is an academic researcher from École Polytechnique Fédérale de Lausanne. The author has contributed to research in topics: Lymphatic system & Lymphangiogenesis. The author has an hindex of 94, co-authored 334 publications receiving 39086 citations. Previous affiliations of Michael Detmar include Harvard University & Beth Israel Deaconess Medical Center.
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Journal ArticleDOI
Mechanisms of Tumor-Induced Lymphovascular Niche Formation in Draining Lymph Nodes.
Catharina D. Commerford,Lothar C. Dieterich,Yuliang He,Tanja Hell,Javier A. Montoya-Zegarra,Simon Flyvbjerg Noerrelykke,Erica Russo,Martin Röcken,Michael Detmar +8 more
TL;DR: Investigation of morphological and molecular changes associated with the lymphatic remodeling process using 4T1 breast cancer and B16F10 melanoma models identifies specific responses of LN LECs to tumor stimuli and provides insights into the mechanisms of lymphovascular niche formation in tumor-draining LNs.
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Activation of the VEGFC/VEGFR3 Pathway Induces Tumor Immune Escape in Colorectal Cancer
Carlotta Tacconi,Federica Ungaro,Carmen Correale,V. Arena,Luca Massimino,Michael Detmar,Antonino Spinelli,Michele Carvello,Massimiliano Mazzone,Ana Isabel Oliveira,Federica Rubbino,Valentina Garlatti,Salvatore Spanò,Enrico Lugli,Federico Colombo,Alberto Malesci,Laurent Peyrin-Biroulet,Stefania Vetrano,Silvio Danese,Silvia D'Alessio +19 more
TL;DR: It is discovered that the VEGFC/VEGFR3 axis can shape both lymphatic endothelial cells (LECs) and TAMs to synergistically inhibit anti-tumor immunity and promote primary CRC growth.
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The Orphan Adhesion G Protein-coupled Receptor GPR97 Regulates Migration of Lymphatic Endothelial Cells via the Small GTPases RhoA and Cdc42
TL;DR: This first evidence that adhesion GPCRs govern LEC motility opens new possibilities for modulating lymphangiogenesis and suggests a possible role of GPR97 in lymphatic remodeling.
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Stroma formation and angiogenesis by overexpression of growth factors, cytokines, and proteolytic enzymes in human skin grafted to SCID mice.
Claus J. Gruss,Kapaettu Satyamoorthy,Carola Berking,John Lininger,Mark Nesbit,Helmut Schaider,Zhao June Liu,Masahiro Oka,Mei-Yu Hsu,Takashi Shirakawa,Gang Li,Thomas Bogenrieder,Peter Carmeliet,Wafik S. El-Deiry,Stephen L. Eck,Justi S. Rao,Andrew H. Baker,Jean T. Bennet,Timothy M. Crombleholme,Omaida C. Velazquez,Omaida C. Velazquez,Jagajan Karmacharya,David J. Margolis,James M. Wilson,Michael Detmar,Mihaela Skobe,Paul D. Robbins,Clayton A. Buck,Meenhard Herlyn +28 more
TL;DR: It is suggested that adenoviral vectors can effectively remodel the architecture of human skin for studies in morphogenesis, inflammatory skin disorders, wound healing, and cancer development.
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Induced lymphatic sinus hyperplasia in sentinel lymph nodes by VEGF-C as the earliest premetastatic indicator
TL;DR: Results suggest that primary tumors -via secretion of VEGF-C- can induce hyperplasia of the sentinel lymph node lymphatic vessel network and thereby promote their further spread and may provide a new prognostic indicator and target for aggressive diseases.