Publications by authors named "Mark Winderlich"

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Correction to: RE‑MIND2: comparative effectiveness of tafasitamab plus lenalidomide versus polatuzumab vedotin/bendamustine/rituximab (pola‑BR), CAR‑T therapies, and lenalidomide/rituximab (R2) based on real‑world data in patients with relapsed/refractory diffuse large B‑cell lymphoma.
Grzegorz S Nowakowski, Dok Hyun Yoon, Patrizia Mondello, Erel Joffe, Anthea Peters, Mark Winderlich

Ann Hematol· September 2023

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RE-MIND2: comparative effectiveness of tafasitamab plus lenalidomide versus polatuzumab vedotin/bendamustine/rituximab (pola-BR), CAR-T therapies, and lenalidomide/rituximab (R2) based on real-world data in patients with relapsed/refractory diffuse large B-cell lymphoma.
Grzegorz S Nowakowski, Dok Hyun Yoon, Patrizia Mondello, Erel Joffe, Anthea Peters, Mark Winderlich

Ann Hematol· July 2023

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Improved Efficacy of Tafasitamab plus Lenalidomide versus Systemic Therapies for Relapsed/Refractory DLBCL: RE-MIND2, an Observational Retrospective Matched Cohort Study.
Grzegorz S Nowakowski, Dok Hyun Yoon, Anthea Peters, Patrizia Mondello, Erel Joffe, Mark Winderlich

Clin Cancer Res· September 2022

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A phase 2a, single-arm, open-label study of tafasitamab, a humanized, Fc-modified, anti-CD19 antibody, in patients with relapsed/refractory B-precursor cell acute lymphoblastic leukemia.
Rebecca B Klisovic, Wing H Leung, Wolfram Brugger, Maren Dirnberger-Hertweck, Mark Winderlich

Cancer· November 2021

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RE-MIND: Comparing Tafasitamab + Lenalidomide (L-MIND) with a Real-world Lenalidomide Monotherapy Cohort in Relapsed or Refractory Diffuse Large B-cell Lymphoma.
Pier Luigi Zinzani, Thomas Rodgers, Dario Marino, Maurizio Frezzato, Anna Maria Barbui, Mark Winderlich

Clin Cancer Res· November 2021

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MOR202, a novel anti-CD38 monoclonal antibody, in patients with relapsed or refractory multiple myeloma: a first-in-human, multicentre, phase 1-2a trial.
Marc S Raab, Monika Engelhardt, Antje Blank, Hartmut Goldschmidt, Hermine Agis, Mark Winderlich

Lancet Haematol· May 2020

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Leukocyte extravasation and vascular permeability are each controlled in vivo by different tyrosine residues of VE-cadherin.
Florian Wessel, Mark Winderlich, Maren Holm, Maike Frye, Ronmy Rivera-Galdos

Nat Immunol· March 2014

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Dissociation of VE-PTP from VE-cadherin is required for leukocyte extravasation and for VEGF-induced vascular permeability in vivo.
Andre Broermann, Mark Winderlich, Helena Block, Maike Frye, Jan Rossaint

J Exp Med· November 2011

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VE-PTP controls blood vessel development by balancing Tie-2 activity.
Mark Winderlich, Linda Keller, Giuseppe Cagna, Andre Broermann, Olena Kamenyeva

J Cell Biol· May 2009

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Cell adhesion dynamics at endothelial junctions: VE-cadherin as a major player.
Dietmar Vestweber, Mark Winderlich, Giuseppe Cagna, Astrid F Nottebaum

Trends Cell Biol· January 2009

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VE-PTP maintains the endothelial barrier via plakoglobin and becomes dissociated from VE-cadherin by leukocytes and by VEGF.
Astrid F Nottebaum, Giuseppe Cagna, Mark Winderlich, Alexander C Gamp, Ruth Linnepe

J Exp Med· November 2008

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Angiopoietins assemble distinct Tie2 signalling complexes in endothelial cell-cell and cell-matrix contacts.
Pipsa Saharinen, Lauri Eklund, Juho Miettinen, Riikka Wirkkala, Andrey Anisimov, Mark Winderlich

Nat Cell Biol· May 2008

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