Fiona Spreitzer

Alexandra Hörmann 2 collaborations

Maja Corcokovic 2 collaborations

Anna Köferle 2 collaborations

Alexandra Popa 2 collaborations

Sarah Oberndorfer 2 collaborations

Ralph A Neumüller 2 collaborations

Johannes Popow 2 collaborations

Thomas Hoffmann 1 collaboration

Jakub Zmajkovic 1 collaboration

Matthias Hinterndorfer 1 collaboration

Jasko Salkanovic 1 collaboration

Katrin Gitschtaler 1 collaboration

Florian Andersch 1 collaboration

Markus Schaefer 1 collaboration

Michaela Fellner 1 collaboration

Nicole Budano 1 collaboration

Jan G Ruppert 1 collaboration

Paolo Chetta 1 collaboration

Melanie Wurm 1 collaboration

Johannes Zuber 1 collaboration

Birgit Wilding 1 collaboration

Lydia Woelflingseder 1 collaboration

Anke Baum 1 collaboration

Krzysztof Chylinski 1 collaboration

Gintautas Vainorius 1 collaboration

Neil Gibson 1 collaboration

Irene C Waizenegger 1 collaboration

Daniel Gerlach 1 collaboration

Martin Augsten 1 collaboration

Yukina Shirai 1 collaboration

Masachika Ikegami 1 collaboration

Sylvia Tilandyova 1 collaboration

Dirk Scharn 1 collaboration

Mark A Pearson 1 collaboration

Anna C Obenauf 1 collaboration

Noboru Yamamoto 1 collaboration

Shunsuke Kondo 1 collaboration

Frans L Opdam 1 collaboration

Annemarie Bruining 1 collaboration

Shinji Kohsaka 1 collaboration

Norbert Kraut 1 collaboration

John V Heymach 1 collaboration

Flavio Solca 1 collaboration

Ralph A Neumuller 1 collaboration

Andreas Schlattl 1 collaboration

Venu Thatikonda 1 collaboration

Madhwesh C Ravichandran 1 collaboration

Verena Supper 1 collaboration

Teresa Puchner 1 collaboration

Corinna Wieshofer 1 collaboration

Christoph Reiser 1 collaboration

Simon Wöhrle 1 collaboration

Mark Pearson 1 collaboration

Javier Martinez 1 collaboration

Stefan Weitzer 1 collaboration

Barbara Mair 1 collaboration

Affiliations

Publications (3)

Precision RNAi using synthetic shRNAmir target sites.

Zongertinib (BI 1810631), an irreversible HER2 TKI, spares EGFR signaling and improves therapeutic response in preclinical models and patients with HER2-driven cancers.

Interrogation of cancer gene dependencies reveals paralog interactions of autosome and sex chromosome-encoded genes.

Réseau de co-auteurs