Contents of Supplementary Tables from 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 M.; Tarantino, Giuseppe; Bryde, Tenna Holgersen; Vijay, Vindhya; Kammula, Ashwin V.; Kattel, Prabhat; Zhu, Songli; Vu, Phuong; Chan, Marina; Wu, Meng-Ju; Gordan, John D.; Patra, Krushna C.; Silveira, Vanessa S.; Manguso, Robert T.; Wein, Marc N.; Ott, Christopher J.; Qi, Jun; Liu, David; Sakamoto, Kei; Gujral, Taranjit S.; Bardeesy, Nabeel

doi:10.1158/2159-8290.28459200

Contents of Supplementary Tables from DNAJB1-PRKACA Fusion Drives Fibrolamellar Liver Cancer through Impaired SIK Signaling and CRTC2/p300-Mediated Transcriptional Reprogramming

journal contribution

posted on 2025-02-21, 18:20 authored by Ilaria Gritti, Jinkai Wan, Vajira Weeresekara, Joel M. Vaz, Giuseppe Tarantino, Tenna Holgersen Bryde, Vindhya Vijay, Ashwin V. Kammula, Prabhat Kattel, Songli Zhu, Phuong Vu, Marina Chan, Meng-Ju Wu, John D. Gordan, Krushna C. Patra, Vanessa S. Silveira, Robert T. Manguso, Marc N. Wein, Christopher J. Ott, Jun Qi, David Liu, Kei Sakamoto, Taranjit S. Gujral, Nabeel Bardeesy

<p>List of contents of each Supplementary Table</p>

Funding

National Cancer Institute (NCI)

United States Department of Health and Human Services

Find out more...

Alex’s Lemonade Stand Foundation for Childhood Cancer (ALSF)

Fibrolamellar Cancer Foundation (FCF)

Bertarelli Rare Cancers Fund

Novo Nordisk Fonden (NNF)

American-Italian Cancer Foundation (AICF)

History

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DOI - Is supplement to DNAJB1-PRKACA Fusion Drives Fibrolamellar Liver Cancer through Impaired SIK Signaling and CRTC2/p300-Mediated Transcriptional Reprogramming

ARTICLE ABSTRACT

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.