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To address this issue, we performed exome and transcriptome sequencing with formalin\u2010fixed paraffin\u2010embedded (FFPE) samples from the NB, PCC, and mixed lesions in a patient with a composite tumor. Whole\u2010exome sequencing revealed that most mutations (80%) were shared by all samples, indicating that NB and PCC evolved from the same clone. Notably, all samples harbored both mutation and focal amplification in the <jats:italic>FGFR1<\/jats:italic> oncogene, resulting in an extraordinarily high expression, likely to be the main driver of this tumor. Transcriptome sequencing revealed undifferentiated expression profiles for the NB lesions. Considering that a metastatic lesion was also composite, most likely, the primitive founding lesions should differentiate into both NB and PCC. This is the first reported case with composite\u2010NB and PCC genetically proven to harbor an oncogenic <jats:italic>FGFR1<\/jats:italic> alteration of a common cellular origin.<\/jats:p>","DOI":"10.1111\/cas.15260","type":"journal-article","created":{"date-parts":[[2021,12,31]],"date-time":"2021-12-31T14:49:47Z","timestamp":1640962187000},"page":"1535-1541","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Oncogenic <i>FGFR1<\/i> mutation and amplification in common cellular origin in a composite tumor with neuroblastoma and pheochromocytoma"],"prefix":"10.1111","volume":"113","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2708-3876","authenticated-orcid":false,"given":"Keiji","family":"Tasaka","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Graduate School of Medicine Kyoto University  Kyoto 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