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We confirmed that a large proportion of patients with cLM have germline FH variants and additionally showed that somatic alteration of FH also drives cLM, with biallelic inactivation of FH being a frequent event. Treatment of Fh1-proficient and -deficient cell lines with the purine antagonist and chemotherapeutic agent, mercaptopurine, significantly decreased growth\/colony formation; however, the addition of nucleosides was able to rescue only the Fh1-proficient cells, suggesting that purine metabolism is a targetable vulnerability for FH-deficient cLMs.<\/jats:p>","DOI":"10.1093\/bjd\/ljae432","type":"journal-article","created":{"date-parts":[[2024,11,7]],"date-time":"2024-11-07T08:08:16Z","timestamp":1730966896000},"page":"551-553","source":"Crossref","is-referenced-by-count":1,"title":["Exploration of the mutational landscape of cutaneous leiomyoma confirms <i>FH<\/i> as a driver gene and identifies targeting purine metabolism as a potential therapeutic strategy"],"prefix":"10.1093","volume":"192","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0645-1879","authenticated-orcid":false,"given":"Louise","family":"van der Weyden","sequence":"first","affiliation":[{"name":"Wellcome Sanger 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