Clinicopathologic and molecular mutational analysis of inflammatory fibroid polyps.J Formos Med Assoc 2025 Jun 10. [Online ahead of print]JF
OBJECTIVE
To study the clinicopathologic features, molecular mutations, as well as the potential cellular origin of the inflammatory fibroid polyps (IFPs).
METHODS
We retrospectively analyzed 97 IFPs from 91 patients at Nanjing Drum Tower Hospital between 2005 and 2018. The clinical and pathological features were compared between gastric IFPs and non-gastric IFPs. Immunohistochemistry of mesenchymal markers (including PDGFRα, DOG1, CD34, SMA, and et al.), and molecular mutational analysis of PDGFRA were carried out. To explore the potential cellular origin of IFPs, the telocyte marker FOXL1 and the trophocyte marker CD81 were detected among those IFPs.
RESULTS
IFPs tended to occur in middle-aged and elderly people, with no significant gender predominance. Microscopically, the presence of "onionskin-like" arrangement, lymphoid follicles was significantly more frequently in the stomach rather than those in the small intestine or colon (P < 0.001 and P = 0.012, respectively). However, hyaline vessels were more common in non-gastric IFPs (P < 0.001). Immunohistochemically, all IFPs showed the expression of PDGFRα, while CD34 may be more frequently lost in the non-gastric IFPs (P = 0.007). PDGFRA mutations were dominant in IFPs larger than 1 cm (P < 0.001). Molecularly, mutations in exon 18 in the kinase domain were frequently identified in stomach, while mutations in exons 10 and 12, located in the transmembrane or juxtamembrane domain were more commonly observed in small intestine (P < 0.001). Immunofluorescence staining showed the presence of the telocyte marker FOXL1 underlying the upper glands. In contrast, the trophocyte marker CD81 was expressed beneath the bottom glands and all IFPs exhibited a more diffuse expression of CD81 compared to FOXL1.
CONCLUSIONS
Gastric and non-gastric IFPs showed different histological and immunohistochemical features, as well as different PDGFRA gene domain mutation, though they may all originated from mesenchymal trophocytes characterized by diffuse CD81 expression.
