Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma

Our preclinical study identifies WEE1-mediated replication stress tolerance as molecular vulnerability in FUS::DDIT3-driven MLS tumorigenesis that could represent a novel target for therapeutic intervention.

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Publication Details

Journal
Clinical Cancer Research
Published
2024-08-29
DOI
https://doi.org/10.1158/1078-0432.ccr-24-1152
Citations
1
Primary Topic
Protein Degradation and Inhibitors
Type
article
Field-Weighted Citation Impact
0.23

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article

Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma

Stefan Fröhling, Wolfgang Hartmann, Claudia Rössig, Kwang Seok Lee et al.
1 citations
Clinical Cancer Research
Protein Degradation and Inhibitors
0.23
article

Exploiting WEE1 Kinase Activity as FUS::DDIT3-Dependent Therapeutic Vulnerability in Myxoid Liposarcoma

Stefan Fröhling, Wolfgang Hartmann, Claudia Rössig, Kwang Seok Lee, Bianca Altvater, Pierre Åman, Marcel Trautmann, Susanne Häfner, Claudia Scholl, Eva Wardelmann, Ilka Isfort, Ruth Berthold, Anna Kuntze, Svenja Wosnig, Lorena Heinst
article en
1 citations

Abstract

Our preclinical study identifies WEE1-mediated replication stress tolerance as molecular vulnerability in FUS::DDIT3-driven MLS tumorigenesis that could represent a novel target for therapeutic intervention.

Clinical Cancer ResearchVol. 30(21)
German Cancer Research Center (DE), Heidelberg University (DE), Sahlgrenska University Hospital (SE), University Hospital Heidelberg (DE), University Hospital Münster (DE), National Center for Tumor Diseases (DE), Institute of Human Genetics (PL), University Hospital Ulm (DE), FH Münster University of Applied Sciences (DE), University of Gothenburg (SE)
Deutsche Forschungsgemeinschaft, Deutsche Krebshilfe
Good health and well-being
Openalex Percentile: Top 43%
Protein Degradation and Inhibitors
0.23
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