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DNAJB1-PRKACA Fusion Drives Fibrolamellar Liver Cancer through Impaired SIK Signaling and CRTC2/p300-Mediated Transcriptional Reprogramming.
- Gritti, Ilaria;
- Wan, Jinkai;
- Weeresekara, Vajira;
- Vaz, Joel;
- Tarantino, Giuseppe;
- Bryde, Tenna;
- Vijay, Vindhya;
- Kammula, Ashwin;
- Kattel, Prabhat;
- Zhu, Songli;
- Vu, Phuong;
- Chan, Marina;
- Wu, Meng-Ju;
- Gordan, John;
- Patra, Krushna;
- Silveira, Vanessa;
- Manguso, Robert;
- Wein, Marc;
- Ott, Christopher;
- Qi, Jun;
- Liu, David;
- Sakamoto, Kei;
- Gujral, Taranjit;
- Bardeesy, Nabeel
- et al.
Published Web Location
https://doi.org/10.1158/2159-8290.CD-24-0634Abstract
This work combines functional studies in model systems and examination of human tumor specimens to define a central oncogenic pathway driven by DNAJB1-PRKACA fusions in FLC. DNAJB1-PRKACA-mediated inactivation of the SIK stimulates CRTC2-p300-mediated transcription to drive tumor growth. The findings illuminate pathogenic mechanisms and inform therapeutic development.
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