Journal
SEMINARS IN CANCER BIOLOGY
Volume 50, Issue -, Pages 115-123Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcancer.2017.11.006
Keywords
Targeted therapies; Fusion transcription factors; PAX3-FOXO1; Alveolar rhabdomyosarcoma; Post-translational modifications; Protein turnover
Categories
Funding
- Swiss National Science Foundation [310030_156923, 31003A_138460]
- Swiss Cancer League [KLS-3868-02-2016, KLS-2784-02-2011]
- Childhood Cancer Research Foundation Switzerland
- Krebsliga Kt. Zurich
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Driver oncogenes are prime targets for therapy in tumors many of which, including leukemias and sarcomas, express recurrent fusion transcription factors. One specific example for such a cancer type is alveolar rhabdomyosarcoma, which is associated in the majority of cases with the fusion protein PAX3-FOXO1. Since fusion transcription factors are challenging targets for development of small molecule inhibitors, indirect inhibitory strategies for this type of oncogenes represent a more promising approach. One can envision strategies at different molecular levels including upstream modifiers and activators, epigenetic and transcriptional co-regulators, and downstream effector targets. In this review, we will discuss the current knowledge regarding potential therapeutic targets that might contribute to indirect interference with PAX3-FOXO1 activity in alveolar rhabdomyosarcoma at the different molecular levels and extrapolate these findings to fusion transcription factors in general.
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