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Lineage infidelity in FH-deficient RCC with secondary somatic alterations: a case report and implications for diagnosis and treatment

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Abstract

Fumarate hydratase (FH)-deficient renal cell carcinoma (RCC) can exhibit striking histologic and immunophenotypic heterogeneity. A 36-year-old woman with uterine leiomyomas presented with a 5.1-cm left renal sinus mass and retroperitoneal adenopathy. Biopsy showed juxtaposed lower-grade oncocytic (PAX8 strong, GATA3 weak) and higher-grade pleomorphic (PAX8 negative, GATA3 and CK7 strong) components. DNA sequencing revealed germline pathogenic FH p.S419P, clonal TP53 p.H193D, and subclonal NF2 and KMT2A mutations, establishing FH-deficient RCC associated with hereditary leiomyomatosis and renal cell carcinoma syndrome. Nivolumab + cabozantinib reduced the lesion before nephrectomy, which showed predominantly pleomorphic tumor cells that were PAX8 negative and GATA3/p63 positive, mimicking upper tract urothelial carcinoma. Transcriptome sequencing mapped the tumor midway between renal and bladder cancer. Postoperatively, nivolumab + ipilimumab with radiotherapy achieved disease control. In this hypothesis-generating case report, TP53, NF2, and KMT2A secondary alterations on an FH-null background were associated with lineage infidelity, which can create diagnostic challenges that underscores the role for integrated pre- and post-treatment multi-omics in diagnostically ambiguous renal tumors.

Original languageEnglish (US)
JournalTherapeutic Advances in Medical Oncology
Volume18
DOIs
StatePublished - Jan 1 2026

Keywords

  • case report
  • fumarate hydratase-deficient renal cell carcinoma
  • hereditary leiomyomatosis
  • immunoradiotherapy
  • lineage infidelity
  • tumor evolution

ASJC Scopus subject areas

  • Oncology

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