ArticlePathology oncology research : POR2013
Molecular characteristics of fibrolamellar hepatocellular carcinoma.
Article in Pathology oncology research : POR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- A framework for fibrolamellar carcinoma research and clinical trials.Nature reviews. Gastroenterology & hepatology · 2022Review
- Comprehensive analysis of The Cancer Genome Atlas reveals a unique gene and non-coding RNA signature of fibrolamellar carcinoma.Scientific reports · 2017Article
- Hepatocellular Carcinoma, Fibrolamellar Variant: Diagnostic Pathologic Criteria and Molecular Pathology Update. A Primer.Diagnostics (Basel, Switzerland) · 2015Article
- Model of fibrolamellar hepatocellular carcinomas reveals striking enrichment in cancer stem cells.Nature communications · 2015Article
- Unique genomic profile of fibrolamellar hepatocellular carcinoma.Gastroenterology · 2015Article
- The genomic landscape of fibrolamellar hepatocellular carcinoma: whole genome sequencing of ten patients.Oncotarget · 2015Article
- Hepatocellular carcinoma with both fibrolamellar and classical components: an unusual morphological pattern.Case reports in pathology · 2015Article
- Detection of a recurrent DNAJB1-PRKACA chimeric transcript in fibrolamellar hepatocellular carcinoma.Science (New York, N.Y.) · 2014Article
- A young woman with liver cancer.Gastrointestinal cancer research : GCR · 2013Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrolamellar hepatocellular carcinoma (FLC) occurs in non-cirrhotic liver and the etiopathogenesis is still obscure. Both hepatocellular and cholangiocellular markers are expressed in the tumor, however, molecular alterations and altered pathways playing role in the tumor pathogenesis are not clearly identified. The purpose of the present study was to compare the expression level of EGFR, syndecan-1 and ß-catenin in FLC, conventional hepatocellular carcinoma (cHCC) and cholangiocellular carcinoma (CCC) and to investigate the possibility of mutation both in EGFR and K-RAS. Eight FLCs were compared with 7 cHCCs, 7 CCCs and 5 normal liver samples. Cytokeratins 7, 8, 18, 19, HepPar1 (HSA), EGFR, syndecan-1 (CD138) and ß-catenin were detected by immunohistochemistry. In addition EGFR, ß-catenin and syndecan-1 were evaluated by digital morphometry and K-RAS, EGFR mutations in FLC cases using paraffin-embedded samples. All FLCs were positive for HepPar1 (HSA) and cytokeratins 7, 8, 18, but negative for cytokeratin 19 by immunohistochemistry. EGFR was significantly overexpressed in all three tumor types, being highest in FLCs (p = 0,0001). EGFR, K-RAS mutation analyses revealed no mutations in exons studied in FLCs. Our findings proved that expression of EGFR is higher in FLC than in other types of primary malignant hepatic tumors and no K-RAS mutation can be detected, so FLC is a good candidate for anti-EGFR treatment.
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