作者
Elana P Simon, Catherine A Freije, Benjamin A Farber, Gadi Lalazar, David G Darcy, Joshua N Honeyman, Rachel Chiaroni-Clarke, Brian D Dill, Henrik Molina, Umesh K Bhanot, Michael P La Quaglia, Brad R Rosenberg, Sanford M Simon
发表日期
2015/11/3
期刊
Proceedings of the National Academy of Sciences
卷号
112
期号
44
页码范围
E5916-E5925
出版商
National Academy of Sciences
简介
Fibrolamellar hepatocellular carcinoma (FLHCC) tumors all carry a deletion of ∼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 (log2 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 …
引用总数
20152016201720182019202020212022202320241718149191415153
学术搜索中的文章
EP Simon, CA Freije, BA Farber, G Lalazar, DG Darcy… - Proceedings of the National Academy of Sciences, 2015