CoChat
Sign Up
Cited by 20Hepatocellular Carcinoma Treatment and PrognosisChromatin Remodeling and CancerSignaling Pathways in Disease

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

Open access
Gritti, Ilaria, Wan, Jinkai, Weeresekara, Vajira, Vaz, Joel M., Tarantino, Giuseppe, Bryde, Tenna Holgersen, Vijay, Vindhya, Kammula, Ashwin V. +16 more·2025·Cancer Discovery
DOI 10.1158/2159-8290.cd-24-0634PMC PMC11803398

Published version of a preprint

Open this paper in CoChat — free accountOpen PDF

Abstract

Fibrolamellar carcinoma (FLC) is a liver cancer of adolescents and young adults characterized by fusions of the genes encoding the protein kinase A catalytic subunit, PRKACA, and heat shock protein, DNAJB1. The chimeric DNAJB1-PRKACA protein has increased kinase activity and is essential for FLC xenograft growth. Here, we explore the critical oncogenic pathways controlled by DNAJB1-PRKACA using patient-derived FLC models, engineered systems, and patient samples. We show that a core function of DNAJB1-PRKACA is the phosphorylation and inactivation of salt-inducible kinases (SIKs). This leads to deregulation of the CRTC2 transcriptional coactivator and p300 acetyltransferase, resulting in transcriptional reprogramming and increased global histone acetylation, driving malignant growth. Our studies establish a central oncogenic mechanism of DNAJB1-PRKACA and suggest the potential of targeting CRTC2/p300 in FLC. Notably, these findings link this rare cancer’s signature fusion oncoprotein to more common cancer gene alterations involving STK11 and GNAS, which also function via SIK suppression. Significance: 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.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1158/2159-8290.cd-24-0634

Cites

4 of 4 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Decreased expression of CRTC2/CREB target genes repressed by active LKB1-SIK signaling was confirmed in isogenic LKB1-expressing xenograft tumors compared to the LKB1-null controls.

    “we measured the level of several CRTC2/CREB target genes that are repressed by active LBK1-SIK signaling in tumors34, confirming decreased gene expression in isogenic LKB1-expressing xenograft tumors compared to the LKB1-null controls (Fig. S4B).”

    From LKB1 regulates JNK-dependent stress signaling and apoptotic dependency of KRAS-mutant lung cancers (2025) · cites this paper as [34]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 64

  1. [1]Ang CS, Kelley RK, Choti MA, Cosgrove DP, Chou JF, Klimstra D, Clinicopathologic characteristics and survival outcomes of patients with fibrolamellar carcinoma: data from the fibrolamellar carcinoma consortium. Gastrointestinal cancer research: GCR 2013; 6(1): 3– 9. 23505572 PMC3597938
  2. [2]O’Neill AF, Church AJ, Perez-Atayde AR, Shaikh R, Marcus KJ, Vakili K. Fibrolamellar carcinoma: An entity all its own. Curr Probl Cancer 2021; 45(4): 100770 doi 10.1016/j.currproblcancer.2021.100770. 34272087 · DOI
  3. [3]Zack T, Losert KP, Maisel SM, Wild J, Yaqubie A, Herman M, Defining incidence and complications of fibrolamellar liver cancer through tiered computational analysis of clinical data. NPJ Precis Oncol 2023; 7(1): 29 doi 10.1038/s41698-023-00371-2. 36959495 PMC10034241 · DOI
  4. [4]Graham RP, Torbenson MS. Fibrolamellar carcinoma: A histologically unique tumor with unique molecular findings. Semin Diagn Pathol 2017; 34(2): 146– 52 doi 10.1053/j.semdp.2016.12.010. 28110996 · DOI
  5. [5]Honeyman JN, Simon EP, Robine N, Chiaroni-Clarke R, Darcy DG, Lim II, Detection of a recurrent DNAJB1-PRKACA chimeric transcript in fibrolamellar hepatocellular carcinoma. Science 2014; 343(6174): 1010– 4 doi 10.1126/science.1249484. 24578576 PMC4286414 · DOI
  6. [6]Singhi AD, Wood LD, Parks E, Torbenson MS, Felsenstein M, Hruban RH, Recurrent Rearrangements in PRKACA and PRKACB in Intraductal Oncocytic Papillary Neoplasms of the Pancreas and Bile Duct. Gastroenterology 2020; 158(3): 573– 82 e2 doi 10.1053/j.gastro.2019.10.028. 31678302 PMC7010554 · DOI
  7. [7]Vyas M, Hechtman JF, Zhang Y, Benayed R, Yavas A, Askan G, DNAJB1-PRKACA fusions occur in oncocytic pancreatic and biliary neoplasms and are not specific for fibrolamellar hepatocellular carcinoma. Mod Pathol 2020; 33(4): 648– 56 doi 10.1038/s41379-019-0398-2. 31676785 PMC7125037 · DOI
  8. [8]Ramms DJ, Raimondi F, Arang N, Herberg FW, Taylor SS, Gutkind JS. Galphas-Protein Kinase A (PKA) Pathway Signalopathies: The Emerging Genetic Landscape and Therapeutic Potential of Human Diseases Driven by Aberrant Galphas-PKA Signaling. Pharmacol Rev 2021; 73(4): 155– 97 doi 10.1124/pharmrev.120.000269. 34663687 PMC11060502 · DOI
  9. [9]Turnham RE, Scott JD. Protein kinase A catalytic subunit isoform PRKACA; History, function and physiology. Gene 2016; 577(2): 101– 8 doi 10.1016/j.gene.2015.11.052. 26687711 PMC4713328 · DOI
  10. [10]Chan GKL, Maisel S, Hwang YC, Pascual BC, Wolber RRB, Vu P, Oncogenic PKA signaling increases c-MYC protein expression through multiple targetable mechanisms. Elife 2023; 12 doi 10.7554/eLife.69521. PMC9925115 36692000 · DOI
  11. [11]Turnham RE, Smith FD, Kenerson HL, Omar MH, Golkowski M, Garcia I, An acquired scaffolding function of the DNAJ-PKAc fusion contributes to oncogenic signaling in fibrolamellar carcinoma. Elife 2019; 8 doi 10.7554/eLife.44187. PMC6533061 31063128 · DOI
  12. [12]Lauer SM, Omar MH, Golkowski MG, Kenerson HL, Lee KS, Pascual BC, Recruitment of BAG2 to DNAJ-PKAc scaffolds promotes cell survival and resistance to drug-induced apoptosis in fibrolamellar carcinoma. Cell Rep 2024; 43(2): 113678 doi 10.1016/j.celrep.2024.113678. 38236773 PMC10964278 · DOI
  13. [13]Kastenhuber ER, Lalazar G, Houlihan SL, Tschaharganeh DF, Baslan T, Chen CC, DNAJB1-PRKACA fusion kinase interacts with beta-catenin and the liver regenerative response to drive fibrolamellar hepatocellular carcinoma. Proc Natl Acad Sci U S A 2017; 114(50): 13076– 84 doi 10.1073/pnas.1716483114. 29162699 PMC5740683 · DOI
  14. [14]Ruland L, Andreatta F, Massalini S, Chuva de Sousa Lopes S, Clevers H, Hendriks D, Organoid models of fibrolamellar carcinoma mutations reveal hepatocyte transdifferentiation through cooperative BAP1 and PRKAR2A loss. Nat Commun 2023; 14(1): 2377 doi 10.1038/s41467-023-37951-6. 37137901 PMC10156813 · DOI
  15. [15]Schalm SS, O’Hearn EE, Wilson K, LaBranche TP, Silva G, Zhang Z, Evaluation of Protein Kinase cAMP-Activated Catalytic Subunit Alpha as a Therapeutic Target for Fibrolamellar Carcinoma. Gastro Hep Advances 2023; 2(3): 307– 21 doi 10.1016/j.gastha.2022.11.004. 39132655 PMC11307690 · DOI
  16. [16]Neumayer C, Ng D, Jiang CS, Qureshi A, Lalazar G, Vaughan R, Oncogenic Addiction of Fibrolamellar Hepatocellular Carcinoma to the Fusion Kinase DNAJB1-PRKACA. Clin Cancer Res 2023; 29(1): 271– 8 doi 10.1158/1078-0432.CCR-22-1851. 36302174 PMC9811160 · DOI
  17. [17]Scott JD, Dessauer CW, Tasken K. Creating order from chaos: cellular regulation by kinase anchoring. Annu Rev Pharmacol Toxicol 2013; 53: 187– 210 doi 10.1146/annurev-pharmtox-011112-140204. 23043438 PMC3540170 · DOI
  18. [19]Sakamoto K, Bultot L, Goransson O. The Salt-Inducible Kinases: Emerging Metabolic Regulators. Trends Endocrinol Metab 2018; 29(12): 827– 40 doi 10.1016/j.tem.2018.09.007. 30385008 · DOI
  19. [20]Darling NJ, Cohen P. Nuts and bolts of the salt-inducible kinases (SIKs). Biochem J 2021; 478(7): 1377– 97 doi 10.1042/BCJ20200502. 33861845 PMC8057676 · DOI
  20. [21]Patel K, Foretz M, Marion A, Campbell DG, Gourlay R, Boudaba N, The LKB1-salt-inducible kinase pathway functions as a key gluconeogenic suppressor in the liver. Nat Commun 2014; 5: 4535 doi 10.1038/ncomms5535. 25088745 PMC4143937 · DOI
  21. [22]Clark K, MacKenzie KF, Petkevicius K, Kristariyanto Y, Zhang J, Choi HG, Phosphorylation of CRTC3 by the salt-inducible kinases controls the interconversion of classically activated and regulatory macrophages. Proc Natl Acad Sci U S A 2012; 109(42): 16986– 91 doi 10.1073/pnas.1215450109. 23033494 PMC3479463 · DOI
  22. [23]Sato T, Andrade CDC, Yoon SH, Zhao Y, Greenlee WJ, Weber PC, Structure-based design of selective, orally available salt-inducible kinase inhibitors that stimulate bone formation in mice. Proc Natl Acad Sci U S A 2022; 119(50): e2214396119 doi 10.1073/pnas.2214396119. 36472957 PMC9897432 · DOI
  23. [24]Viste K, Kopperud RK, Christensen AE, Doskeland SO. Substrate enhances the sensitivity of type I protein kinase a to cAMP. J Biol Chem 2005; 280(14): 13279– 84 doi 10.1074/jbc.M413065200. 15691833 · DOI
  24. [25]Willis BS, Niswender CM, Su T, Amieux PS, McKnight GS. Cell-type specific expression of a dominant negative PKA mutation in mice. PLoS One 2011; 6(4): e18772 doi 10.1371/journal.pone.0018772. 21533282 PMC3075275 · DOI
  25. [26]Sundberg TB, Liang Y, Wu H, Choi HG, Kim ND, Sim T, Development of Chemical Probes for Investigation of Salt-Inducible Kinase Function in Vivo. ACS Chem Biol 2016; 11(8): 2105– 11 doi 10.1021/acschembio.6b00217. 27224444 PMC4992440 · DOI
  26. [28]Rodon L, Svensson RU, Wiater E, Chun MGH, Tsai WW, Eichner LJ, The CREB coactivator CRTC2 promotes oncogenesis in LKB1-mutant non-small cell lung cancer. Sci Adv 2019; 5(7): eaaw6455 doi 10.1126/sciadv.aaw6455. 31355336 PMC6656544 · DOI
  27. [29]Muller-Dott S, Tsirvouli E, Vazquez M, Ramirez Flores RO, Badia IMP, Fallegger R, Expanding the coverage of regulons from high-confidence prior knowledge for accurate estimation of transcription factor activities. Nucleic Acids Res 2023; 51(20): 10934– 49 doi 10.1093/nar/gkad841. 37843125 PMC10639077 · DOI
  28. [30]Zhou X, Li JW, Chen Z, Ni W, Li X, Yang R, Dependency of human and murine LKB1-inactivated lung cancer on aberrant CRTC-CREB activation. Elife 2021; 10 doi 10.7554/eLife.66095. PMC8238510 34142658 · DOI
  29. [31]Wang Y, Vera L, Fischer WH, Montminy M. The CREB coactivator CRTC2 links hepatic ER stress and fasting gluconeogenesis. Nature 2009; 460(7254): 534– 7 doi 10.1038/nature08111. 19543265 PMC2730924 · DOI
  30. [32]Xie F, Li BX, Kassenbrock A, Xue C, Wang X, Qian DZ, Identification of a Potent Inhibitor of CREB-Mediated Gene Transcription with Efficacious in Vivo Anticancer Activity. J Med Chem 2015; 58(12): 5075– 87 doi 10.1021/acs.jmedchem.5b00468. 26023867 PMC4493896 · DOI
  31. [33]Li BX, Gardner R, Xue C, Qian DZ, Xie F, Thomas G, Systemic Inhibition of CREB is Well-tolerated in vivo. Sci Rep 2016; 6: 34513 doi 10.1038/srep34513. 27694829 PMC5046085 · DOI
  32. [34]Cui A, Ding D, Li Y. Regulation of Hepatic Metabolism and Cell Growth by the ATF/CREB Family of Transcription Factors. Diabetes 2021; 70(3): 653– 64 doi 10.2337/dbi20-0006. 33608424 PMC7897342 · DOI
  33. [35]Tasoulas J, Rodon L, Kaye FJ, Montminy M, Amelio AL. Adaptive Transcriptional Responses by CRTC Coactivators in Cancer. Trends Cancer 2019; 5(2): 111– 27 doi 10.1016/j.trecan.2018.12.002. 30755304 PMC9682902 · DOI
  34. [37]Murakami T, Kondo S, Ogata M, Kanemoto S, Saito A, Wanaka A, Cleavage of the membrane-bound transcription factor OASIS in response to endoplasmic reticulum stress. J Neurochem 2006; 96(4): 1090– 100 doi 10.1111/j.1471-4159.2005.03596.x. 16417584 · DOI
  35. [38]Feng YX, Jin DX, Sokol ES, Reinhardt F, Miller DH, Gupta PB. Cancer-specific PERK signaling drives invasion and metastasis through CREB3L1. Nat Commun 2017; 8(1): 1079 doi 10.1038/s41467-017-01052-y. 29057869 PMC5651903 · DOI
  36. [39]Cleary JM, Raghavan S, Wu Q, Li YY, Spurr LF, Gupta HV, FGFR2 Extracellular Domain In-Frame Deletions Are Therapeutically Targetable Genomic Alterations That Function as Oncogenic Drivers in Cholangiocarcinoma. Cancer Discov 2021; 11(10): 2488– 505 doi 10.1158/2159-8290.CD-20-1669. 33926920 PMC8690974 · DOI
  37. [40]Dinh TA, Sritharan R, Smith FD, Francisco AB, Ma RK, Bunaciu RP, Hotspots of Aberrant Enhancer Activity in Fibrolamellar Carcinoma Reveal Candidate Oncogenic Pathways and Therapeutic Vulnerabilities. Cell Rep 2020; 31(2): 107509 doi 10.1016/j.celrep.2020.03.073. 32294439 PMC7474926 · DOI
  38. [41]Sorenson EC, Khanin R, Bamboat ZM, Cavnar MJ, Kim TS, Sadot E, Genome and transcriptome profiling of fibrolamellar hepatocellular carcinoma demonstrates p53 and IGF2BP1 dysregulation. PLoS One 2017; 12(5): e0176562 doi 10.1371/journal.pone.0176562. 28486549 PMC5423588 · DOI
  39. [42]Malouf GG, Job S, Paradis V, Fabre M, Brugieres L, Saintigny P, Transcriptional profiling of pure fibrolamellar hepatocellular carcinoma reveals an endocrine signature. Hepatology 2014; 59(6): 2228– 37 doi 10.1002/hep.27018. 24443104 · DOI
  40. [43]Levin SN, Tomasini MD, Knox J, Shirani M, Shebl B, Requena D, Disruption of proteome by an oncogenic fusion kinase alters metabolism in fibrolamellar hepatocellular carcinoma. Sci Adv 2023; 9(25): eadg7038 doi 10.1126/sciadv.adg7038. 37343102 PMC10284549 · DOI
  41. [44]Daniel SK, Sullivan KM, Dickerson LK, van den Bijgaart RJE, Utria AF, Labadie KP, Reversing immunosuppression in the tumor microenvironment of fibrolamellar carcinoma via PD-1 and IL-10 blockade. Sci Rep 2024; 14(1): 5109 doi 10.1038/s41598-024-55593-6. 38429349 PMC10907637 · DOI
  42. [45]Altarejos JY, Montminy M. CREB and the CRTC co-activators: sensors for hormonal and metabolic signals. Nat Rev Mol Cell Biol 2011; 12(3): 141– 51 doi 10.1038/nrm3072. 21346730 PMC4324555 · DOI
  43. [46]Lasko LM, Jakob CG, Edalji RP, Qiu W, Montgomery D, Digiammarino EL, Discovery of a selective catalytic p300/CBP inhibitor that targets lineage-specific tumours. Nature 2017; 550(7674): 128– 32 doi 10.1038/nature24028. 28953875 PMC6050590 · DOI · Paper page
  44. [47]White J, Derheimer FA, Jensen-Pergakes K, O’Connell S, Sharma S, Spiegel N, Histone lysine acetyltransferase inhibitors: an emerging class of drugs for cancer therapy. Trends Pharmacol Sci 2024; 45(3): 243– 54 doi 10.1016/j.tips.2024.01.010. 38383216 · DOI
  45. [48]Weinert BT, Narita T, Satpathy S, Srinivasan B, Hansen BK, Scholz C, Time-Resolved Analysis Reveals Rapid Dynamics and Broad Scope of the CBP/p300 Acetylome. Cell 2018; 174(1): 231– 44 e12 doi 10.1016/j.cell.2018.04.033. 29804834 PMC6078418 · DOI
  46. [49]Liu Y, Dentin R, Chen D, Hedrick S, Ravnskjaer K, Schenk S, A fasting inducible switch modulates gluconeogenesis via activator/coactivator exchange. Nature 2008; 456(7219): 269– 73 doi 10.1038/nature07349. 18849969 PMC2597669 · DOI
  47. [50]Bricambert J, Miranda J, Benhamed F, Girard J, Postic C, Dentin R. Salt-inducible kinase 2 links transcriptional coactivator p300 phosphorylation to the prevention of ChREBP-dependent hepatic steatosis in mice. J Clin Invest 2010; 120(12): 4316– 31 doi 10.1172/JCI41624. 21084751 PMC2993582 · DOI
  48. [51]Vannam R, Sayilgan J, Ojeda S, Karakyriakou B, Hu E, Kreuzer J, Targeted degradation of the enhancer lysine acetyltransferases CBP and p300. Cell Chem Biol 2021; 28(4): 503– 14 e12 doi 10.1016/j.chembiol.2020.12.004. 33400925 · DOI · Paper page
  49. [52]Andersson R, Sandelin A. Determinants of enhancer and promoter activities of regulatory elements. Nat Rev Genet 2020; 21(2): 71– 87 doi 10.1038/s41576-019-0173-8. 31605096 · DOI · Paper page
  50. [53]Durbin AD, Wang T, Wimalasena VK, Zimmerman MW, Li D, Dharia NV, EP300 Selectively Controls the Enhancer Landscape of MYCN-Amplified Neuroblastoma. Cancer Discov 2022; 12(3): 730– 51 doi 10.1158/2159-8290.CD-21-0385. 34772733 PMC8904277 · DOI
  51. [54]Gao Q, Liang WW, Foltz SM, Mutharasu G, Jayasinghe RG, Cao S, Driver Fusions and Their Implications in the Development and Treatment of Human Cancers. Cell Rep 2018; 23(1): 227– 38 e3 doi 10.1016/j.celrep.2018.03.050. 29617662 PMC5916809 · DOI
  52. [55]Murray CW, Brady JJ, Tsai MK, Li C, Winters IP, Tang R, An LKB1-SIK Axis Suppresses Lung Tumor Growth and Controls Differentiation. Cancer Discov 2019; 9(11): 1590– 605 doi 10.1158/2159-8290.CD-18-1237. 31350327 PMC6825558 · DOI · Paper page
  53. [56]Jagannath A, Butler R, Godinho SIH, Couch Y, Brown LA, Vasudevan SR, The CRTC1-SIK1 pathway regulates entrainment of the circadian clock. Cell 2013; 154(5): 1100– 11 doi 10.1016/j.cell.2013.08.004. 23993098 PMC3898689 · DOI
  54. [57]Lalazar G, Requena D, Ramos-Espiritu L, Ng D, Bhola PD, de Jong YP, Identification of Novel Therapeutic Targets for Fibrolamellar Carcinoma Using Patient-Derived Xenografts and Direct-from-Patient Screening. Cancer Discov 2021; 11(10): 2544– 63 doi 10.1158/2159-8290.CD-20-0872. 34127480 PMC8734228 · DOI
  55. [58]Shebl B, Ng D, Lalazar G, Rosemore C, Finkelstein TM, Migler RD, Targeting BCL-XL in fibrolamellar hepatocellular carcinoma. JCI Insight 2022; 7(17) doi 10.1172/jci.insight.161820. PMC9536265 36073545 · DOI
  56. [59]Compton SE, Kitchen-Goosen SM, DeCamp LM, Lau KH, Mabvakure B, Vos M, LKB1 controls inflammatory potential through CRTC2-dependent histone acetylation. Mol Cell 2023; 83(11): 1872– 86 e5 doi 10.1016/j.molcel.2023.04.017. 37172591 PMC13133714 · DOI
  57. [60]Wu Q, Zhen Y, Shi L, Vu P, Greninger P, Adil R, EGFR Inhibition Potentiates FGFR Inhibitor Therapy and Overcomes Resistance in FGFR2 Fusion-Positive Cholangiocarcinoma. Cancer Discov 2022; 12(5): 1378– 95 doi 10.1158/2159-8290.CD-21-1168. 35420673 PMC9064956 · DOI · Paper page
  58. [61]Dobin A, Davis CA, Schlesinger F, Drenkow J, Zaleski C, Jha S, STAR: ultrafast universal RNA-seq aligner. Bioinformatics 2013; 29(1): 15– 21 doi 10.1093/bioinformatics/bts635. 23104886 PMC3530905 · DOI · Paper page
  59. [62]Li H, Handsaker B, Wysoker A, Fennell T, Ruan J, Homer N, The Sequence Alignment/Map format and SAMtools. Bioinformatics 2009; 25(16): 2078– 9 doi 10.1093/bioinformatics/btp352. 19505943 PMC2723002 · DOI · Paper page
  60. [63]Liao Y, Smyth GK, Shi W. featureCounts: an efficient general purpose program for assigning sequence reads to genomic features. Bioinformatics 2014; 30(7): 923– 30 doi 10.1093/bioinformatics/btt656. 24227677 · DOI · Paper page
  61. [64]Krug K, Mertins P, Zhang B, Hornbeck P, Raju R, Ahmad R, A Curated Resource for Phosphosite-specific Signature Analysis. Mol Cell Proteomics 2019; 18(3): 576– 93 doi 10.1074/mcp.TIR118.000943. 30563849 PMC6398202 · DOI
  62. [65]Robinson MD, McCarthy DJ, Smyth GK. edgeR: a Bioconductor package for differential expression analysis of digital gene expression data. Bioinformatics 2010; 26(1): 139– 40 doi 10.1093/bioinformatics/btp616. 19910308 PMC2796818 · DOI · Paper page
  63. [67]Farshidfar F, Zheng S, Gingras MC, Newton Y, Shih J, Robertson AG, Integrative Genomic Analysis of Cholangiocarcinoma Identifies Distinct IDH-Mutant Molecular Profiles. Cell Rep 2017; 18(11): 2780– 94 doi 10.1016/j.celrep.2017.02.033. 28297679 PMC5493145 · DOI
  64. [68]Cancer Genome Atlas Research Network. Electronic address wbe, Cancer Genome Atlas Research N. Comprehensive and Integrative Genomic Characterization of Hepatocellular Carcinoma. Cell 2017; 169(7): 1327– 41 e23 doi 10.1016/j.cell.2017.05.046. 28622513 PMC5680778 · DOI · Paper page

Cited by

Sorted by citations

Authors
Gritti, I., Wan, J., Weeresekara, V., Vaz, J. M., Tarantino, G., Bryde, T. H., Vijay, V., Kammula, A. V., Kattel, P., Zhu, S., Vu, P., Chan, M., Wu, M.-J., Gordan, J. D., Patra, K. C., Silveira, V. S., Manguso, R. T., Wein, M. N., Ott, C. J., Qi, J., Liu, D., Sakamoto, K., Gujral, T. S., & Bardeesy, N.
Affiliations
  • Broad Institute (US)
  • Fred Hutch Cancer Center (US)
  • University of Copenhagen (DK)
  • Harvard University (US)
  • University of California, San Francisco (US)
  • University of Cincinnati (US)
Corresponding author
  • Gujral, Taranjit S.
  • Bardeesy, Nabeel
ORCID
Venue
Cancer Discovery
Publisher
American Association for Cancer Research (AACR)
Published
2024-09-27
Volume
15
Issue
2
Pages
382-400
ISSN
  • 2159-8274 (ISSN-L)
  • 2159-8290
DOI
10.1158/2159-8290.cd-24-0634
PMC
PMC11803398
OpenAlex
W4402886836
Cited by
20
References
4
Citations by year
2026: 10 · 2025: 10
FWCI
5.24
Type
journal article
Language
en
Update notices
correction (2025-04-02)
Open access
Licence
Locations
  • Cancer Discovery (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • Research at the University of Copenhagen (University of Copenhagen) (publishedVersion, cc-by-nc-nd)
  • eScholarship (California Digital Library) (submittedVersion, cc-by-nc-nd)
Funders
  • National Cancer Institute (P50CA127003, R01CA215498, R01CA219670, P01CA117969, R01CA273081, R01CA279997)
  • Alex’s Lemonade Stand Foundation for Childhood Cancer (21-24687)
  • Fibrolamellar Cancer Foundation
  • Bertarelli Rare Cancers Fund
  • Novo Nordisk Fonden (NNF18CC0034900, NNF23SA0084103)
  • American-Italian Cancer Foundation
Topics
  • Health Sciences › Medicine › Hepatology › Hepatocellular Carcinoma Treatment and Prognosis
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Keywords
fibrolamellar hepatocellular carcinoma, DNAJB1-PRKACA fusion, salt-inducible kinases, CRTC2, P300, histone acetylation, transcriptional reprogramming, fusion oncogenes, STK11, GNAS, liver cancer, kinase inactivation, therapeutic target
MeSH terms
Animals, Carcinoma, Hepatocellular, Humans, Liver Neoplasms, Transcription Factors, Signal Transduction, Oncogene Proteins, Fusion, Gene Expression Regulation, Neoplastic, Protein Serine-Threonine Kinases, Cell Line, Tumor, E1A-Associated p300 Protein, HSP40 Heat-Shock Proteins, Mice, Cyclic AMP-Dependent Protein Kinase Catalytic Subunits

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review