Phosphaturic mesenchymal tumors (PMTs) are rare neoplasms of soft tissue or bone. While previous studies revealed that approximately 50% of PMTs harbored FN1::FGFR1 fusions, the molecular mechanisms in the remaining cases are largely unknown. In this study, fusion genes were investigated using RNA-based next generation sequencing (NGS) in 76 retrospectively collected PMTs. Novel fusions were validated with Sanger sequencing and fluorescence in situ hybridization (FISH). Fusion genes were detected in 52/76 (68.4%) PMTs, and 43/76 (56.6%) harbored FN1::FGFR1 fusions. Fusion transcripts and breakpoints of the FN1::FGFR1 fusions were diverse. The most common fusion transcript was between exon 20 of FN1 and exon 9 of FGFR1 (7/43, 16.3%). The most upstream breakpoint of FN1 gene was located at the 3' end of exon 12, and the most downstream breakpoint of FGFR1 gene was at the 5' end of exon 9, suggesting the inessential nature of the third fibronectin type domain of FN1, and the necessity of the transmembrane domain of FGFR1 in the FN1::FGFR1 fusion protein, respectively. Moreover, the reciprocal FGFR1::FN1 fusions, which had not been identified in previous studies, were detected in 18.6% (8/43) of FN1::FGFR1 fusion-positive PMTs. Novel fusions were identified in 6/76 (7.9%) FN1::FGFR1 fusion-negative PMTs including two involving FGFR: FGFR1::USP33 (1/76, 1.3%), and FGFR1::TLN1 (1/76, 1.3%). Other novel fusions identified were the PDGFRA::USP35 (1/76, 1.3%), SPTBN1::YWHAQ (1/76, 1.3%), GTF2I::RALGPS1 (1/76, 1.3%), and LTBP1::VWA8 (1/76, 1.3%) fusions. In addition to these novel fusions, FN1::FGFR2 fusion (1/76, 1.3%), NIPBL::BEND2 fusion (1/76, 1.3%) and KIAA1549::BRAF fusion (1/76, 1.3%) were also identified in FN1::FGFR1-negative cases arising from thigh, ilium, and acetabulum, respectively. The frequency of oncogenic fusions was significantly higher (p=0.012) in tumors derived from extremities (29/35, 82.9%) compared with other locations (23/41, 56.1%). No significant correlation was identified between fusions and recurrence (p=0.786). In conclusion, we report fusion transcripts and breakpoints of FN1::FGFR1 in PMTs in detail, providing insights into fusion protein functions. We also revealed that a considerable proportion of PMTs without FN1::FGFR1 fusion carried novel fusions, providing further insight into the genetic basis of PMTs.