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Molecular Profiling of the Invasive Tumor Microenvironment in a 3-Dimensional Model of Colorectal Cancer Cells and Ex vivo Fibroblasts
Published on: April 29, 2014
Clinicopathologic and molecular mutational analysis of inflammatory fibroid polyps
Qianyun Shi1, Biao Zhang1, Jun Yang1
1Department of Pathology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing 210008, Jiangsu Province, China.
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.
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