Whole-exome sequencing identified TP53 mutation (c.672+2T>C, involving a splice site, with concomitant protein loss) in a cervical sarcoma, limited to its heterologous liposarcomatous component. CDKN2A homozygous deletion with concomitant p16 loss occurred in 4/7. All cases expressed CD34, while five were S100-positive. Pan-TRK immunostaining was positive in all cases. Abrupt high-grade transformation into pleomorphic liposarcoma was found in another cervical tumor, while the pleural tumor contained intermixed rhabdomyoblasts. Adenosarcoma-like appearances were observed in two, manifesting frond-like protrusions in one cervical tumor and phyllodes-like architecture in the prostatic tumor. Keloid-like stromal collagen and perivascular hyalinization was noted in five. The tumors exhibited spindled to ovoid/epithelioid or pleomorphic cells, often arranged in fascicles, and were low-to-intermediate-grade and high-grade in three and four cases, respectively. In five females and two males aged 18–53 years, we characterized visceral mesenchymal tumors harboring TPM3-NTRK1, LMNA-NTRK1 (lung), SQSTM1-NTRK3 (heart), and NTRK3 rearrangement with unknown fusion partner (colon/mesocolon) with RNA sequencing, FISH, RT-PCR, and immunohistochemistry. Given the responsiveness to selective NTRK inhibitors, it remains critical to identify those ultra-rare cases occurring in the viscera of adults. NTRK-rearranged mesenchymal neoplasms mostly affect the soft tissues of pediatric patients.