ArticleGut2001
Genomic homogeneity in fibrolamellar carcinomas.
Article in Gut, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 20 citations in OpenAlex.
- The genomic landscape of fibrolamellar hepatocellular carcinoma: whole genome sequencing of ten patients.Oncotarget · 2015Article
- Methylome sequencing for fibrolamellar hepatocellular carcinoma depicts distinctive features.Epigenetics · 2015Article
- Molecular characteristics of fibrolamellar hepatocellular carcinoma.Pathology oncology research : POR · 2013Article
- Fibrolamellar carcinoma: 2012 update.Scientifica · 2012Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFibrolamellar carcinoma (FLC) is a variant of hepatocellular carcinoma (HCC) with distinctive clinical and histological features. To date there have been few studies on the genotypic aspects of FLC and no previous attempts have been made to use the arbitrarily primed-polymerase chain reaction (AP-PCR) technique to detect genetic alterations in this disease.
aimThe aim of this study was to assess the degree of genomic heterogeneity of FLC using the AP-PCR technique.
methodsA total of 50 tissue samples of primary and metastatic FLCs from seven patients were microdissected. AP-PCR amplification of each genomic DNA sample was carried out using two arbitrary primers.
resultsDNA fingerprints of the primary FLCs and all their metastatic lesions (both synchronous and metachronous disease) were identical in an individual patient. The fingerprints were different between tumours of different patients. No evidence of intratumour heterogeneity was observed.
conclusionsSuch genomic homogeneity in FLCs may explain their indolent growth. The absence of clonal evolution, which is present in other tumours (particularly HCCs), may explain the distinct behaviour in this tumour. The tumorigenic pathway and degree of somatic genomic changes in this disease may be less complex than in HCC.
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