Clonality and TP53 mutation analysis of focal nodular hyperplasia of the liver

Suqin Zheng, Oscar W. Cummings, Romil Saxena, Shaobo Zhang, Mingsheng Wang, Sean R. Williamson, Monica Cheng, Antonio Lopez-Beltran, Rodolfo Montironi, Kurt B. Hodges, Liang Cheng

Research output: Contribution to journalArticle

5 Scopus citations

Abstract

Focal nodular hyperplasia (FNH) is considered a benign tumor of the liver. However, the biologic nature and clonality status of FNH are not well established. We sought to determine the clonality and TP53 mutation status of FNH to better characterize the nature of FNH. We analyzed 15 cases of FNH from female patients who underwent surgical resection of their lesions. Genomic DNA was extracted from paraffin-embedded tissue sections using laser-capture microdissection and analyzed for X-chromosome inactivation status and TP53 mutations by direct DNA sequencing. Thirteen cases were informative for X-chromosome inactivation analysis. Of the 13 informative cases, 4 (31%) showed a nonrandom pattern of X-chromosome inactivation, consistent with monoclonal origin. No TP53 mutations were detected in any of the FNH cases. The clonality status was not associated with any clinicopathologic parameters such as age and lesion size. Our data indicate that a significant proportion of FNH lesions have a monoclonal origin, suggesting that they are neoplastic rather than reactive.

Original languageEnglish (US)
Pages (from-to)65-70
Number of pages6
JournalAmerican journal of clinical pathology
Volume134
Issue number1
DOIs
StatePublished - Jul 1 2010

Keywords

  • Clonality
  • Focal nodular hyperplasia
  • Liver
  • Microdissection
  • TP53 mutation
  • X-chromosome inactivation

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

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