FET fusion oncoproteins disrupt physiologic DNA repair and create a targetable opportunity for ATR inhibitor therapy

Abstract excerpt

In cancers with genetic loss of specific DNA damage response (DDR) genes (i.e., BRCA1/2 tumor suppressor mutations), synthetic lethal targeting of compensatory DDR pathways has translated into clinical benefit for patients. Whether and how growth-promoting oncogenes might also create tumor-specific vulnerabilities within DDR networks is not well understood. Here we focus on Ewing sarcoma, a FET fusion oncoprotein...

Topics

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• Cancer Genomics and Diagnostics
• Cell death mechanisms and regulation
• DNA Repair Mechanisms
• Lymphoma Diagnosis and Treatment
• PARP inhibition in cancer therapy
• Protein Degradation and Inhibitors
• Sarcoma Diagnosis and Treatment
• Ubiquitin and proteasome pathways

Identifiers and source

Literature Corpus work

1c73f589-761d-5a2c-9c51-819d593ba749

DOI

10.1101/2023.04.30.538578