Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 112, Issue 44, Pages E5916-E5925Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1424894112
Keywords
pediatric cancer; liver cancer; protein kinase; genomics; fusion gene
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Funding
- Fibrolamellar Cancer Foundation
- Sohn Foundation
- Rockefeller University Center for Clinical and Translational Science Grant [2UL1RR024143]
- Cancer Center Support grant from the National Institutes of Health/National Cancer Institute [5P30CA008748]
- Leona M. and Harry B. Helmsley Charitable Trust
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Fibrolamellar hepatocellular carcinoma (FLHCC) tumors all carry a deletion of similar to 400 kb in chromosome 19, resulting in a fusion of the genes for the heat shock protein, DNAJ (Hsp40) homolog, subfamily B, member 1, DNAJB1, and the catalytic subunit of protein kinase A, PRKACA. The resulting chimeric transcript produces a fusion protein that retains kinase activity. No other recurrent genomic alterations have been identified. Here we characterize the molecular pathogenesis of FLHCC with transcriptome sequencing (RNA sequencing). Differential expression (tumor vs. adjacent normal tissue) was detected for more than 3,500 genes (log(2) fold change >= 1, false discovery rate <= 0.01), many of which were distinct from those found in hepatocellular carcinoma. Expression of several known oncogenes, such as ErbB2 and Aurora Kinase A, was increased in tumor samples. These and other dysregulated genes may serve as potential targets for therapeutic intervention.
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