Inflammatory Fibroid Polyps of the Colon: A Study on the Morphological Spectrum, Immunoexpression Characteristics, and Outcomes

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Methods: In this study, We collected nine cases of colonic IFPs and provide a comprehensive description of the clinicopathological features and developmental outcomes of these lesions. Results: These nine cases of colonic IFPs can be classified into four types on the basis of their pathological characteristics: early-stage, classic, inflammatory, and sclerotic. The early-stage type of IFP is characterized by the deposition of fibrosis around blood vessels and between glands. The classic type of IFP is easily identifiable by its "onion-skin-like" structure; however, immunohistochemical (IHC) staining for CD34 may demonstrate focal positivity or even negativity. The inflammatory type of IFP is large and characterized by significant infiltration of plasma cells. IHC staining revealed variable positivity for both CD34 and PDGFRα across different regions of the lesions. The sclerotic type of IFP is characterized by substantial deposition of collagen. Furthermore, our findings suggest that early-stage IFPs have the potential to either develop into classic-type IFPs or degenerate into sclerotic-type IFPs. Additionally, classic-type IFPs may acquire PDGFRα mutations and ultimately transform into inflammatory-type IFPs. Conclusions: Colonic IFPs exhibit a distinct morphological spectrum and unique immunoexpressioncharacteristics as they progress. Only inflammatory-type and classic-type IFPs with PDGFRα mutations or immunoexpression should be regarded as genuine neoplastic lesions. Inflammatory Fibrous Polyp Colon Morphological Spectrum Immunoexpression Outcome Figures Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Introduction In 1949, Vanek first reported six cases of polypoid lesions in the stomach. He described them as submucosal granulomas with eosinophilic infiltration, on the basis of their morphological features ( 1 ). In 1953, Helwig and Ranier introduced the term inflammatory fibrous polyp (IFP) to describe these lesions, a term that has become widely used and accepted ( 2 , 3 ). In a groundbreaking study in 2008, Schildhaus et al. demonstrated that the majority of IFPs possess mutations in the platelet-derived growth factor receptor alpha (PDGFRα) gene, providing evidence that IFPs are genuine neoplastic lesions ( 4 ). As a result, both the fourth edition in 2010 and the fifth edition in 2019 of the World Health Organization's Classification of Tumors of the Digestive System classified IFPs as benign mesenchymal tumors of the digestive system ( 5 , 6 ). IFPs can develop anywhere in the gastrointestinal (GI) tract. They are most commonly found in the stomach (66.7%) and the small intestine (21.1%), as reported previously ( 7 ). Research has shown that the morphological and genetic features of IFPs vary depending on their location in the body. For example, gastric IFPs often exhibit characteristic "onion skin-like" structures, with spindle-shaped or oval-shaped tumor cells arranged in a vortex pattern around blood vessels or mucosal glands. This is often accompanied by the infiltration of eosinophils. In contrast, IFPs in the small intestine typically present a significant presence of mixed inflammatory cells, including eosinophils, lymphocytes, plasma cells, and mast cells. However, the "onion skin-like" structure is uncommon in this location ( 8 ). Furthermore, 53.3% of gastric IFPs carry a PDGFRα gene mutation, with most (68.8%) mutations located in exon 18. In comparison, 58.0% of IFPs in the small intestine carry a mutation in this gene, with the majority (83.0%) of mutations located in exon 12 ( 9 ). Previous studies have shown that the colon is a rare site for IFP, accounting for only 8.4% of all cases ( 7 ). However, in our practical experience, we have observed a greater prevalence of IFP in the colon than in the gastric and small intestine. This study presents nine cases of colonic IFP at various stages of progression, providing a comprehensive overview of the morphological spectrum and immunoexpression characteristics of this lesion. Our findings indicate that only the inflammatory type of IFPs, along with a subset of classic type IFPs exhibiting PDGFRα gene mutations, have the potential for continued growth. Materials and methods Nine cases of colonic IFPs collected between 2014 and 2020 were retrieved from the files of the Department of Pathology at Sun Yat-sen University Seventh Affiliated Hospital. Clinical data for all patients were collected. At least two pathologists reviewed the pathological sections to confirm the diagnosis. The samples were fixed in 4% formaldehyde and embedded in paraffin via standard procedures. Sections measuring 3–4 µm were cut from the tissue blocks and stained with hematoxylin‒eosin (H&E). For immunohistochemical (IHC) staining, the EnVision two-step method was employed. Antigen retrieval was conducted at high temperature. The following primary antibodies were used: CD34 (DAKO, QBEnd 10), CD117 (Roche, 9.7), Desmin (ZSGB-BIO, OTIR4A8), DOG-1 (MXB, SP31), Ki-67 (DAKO, MIB-1), PDGFRα (ZSGB-BIO, ZA-0377), SMA (DAKO, 1A4), and S-100 (DAKO, ZO311). Both positive and negative controls are shown on the slides. Immunopositivity was described as negative (-), focal positive (+) when less than 50% of the cells exhibited staining, and positive (++) when more than 50% of the cells showed staining. H&E- and IHC-stained sections were scanned via the MagScanner (KF-PRO-005). Typical pathological images were captured from the scanned sections. Results Table 1 provides a comprehensive summary of the clinicopathological characteristics of the nine patients with colonic IFPs. Among the nine patients, three were diagnosed with male patients, and six were diagnosed with female patients, resulting in a male-to-female ratio of 1:2. The age range of the patients was 35–66 years, with a median age of 43 years. Four cases were located in the ascending colon, two in the transverse colon, and three in the descending or sigmoid colon. Four patients experienced symptoms such as diarrhea, hematochezia, and abdominal pain. In two patients, endoscopic findings revealed a polypoid mass in the intestinal lumen, whereas the remaining seven patients presented with sessile lesions. Notably, five out of the nine patients had type 2 diabetes. IHC staining for CD117, DOG-1, Desmin, SMA, and S-100 was performed to exclude differential diagnoses, including gastrointestinal stromal tumors (GISTs), smooth muscle tumors, inflammatory myofibroblastic tumors (IMTs), and neural tumors, respectively. These nine cases of colonic IFP can be classified into four types on the basis of their pathological features. Table 1 Clinicopathological (histological & immunohistochemical) features of colonic IFP. Case Sex/age (years) Location(colon) Symptom Size (cm) Diabetes Histologic type IHC CD34 PDGFRα 1 F/44 Ascending None 0.3 Yes Early-stage + - 2 M/36 Descending None 0.2 No Early-stage + - 3 F/35 Ascending None 0.3 Yes Early-stage + - 4 F/39 Transverse Diarrhea 0.4 NK Classic - - 5 M/44 Sigmoid None 0.5 Yes Classic ++ + 6 F/42 Transverse None 0.6 No Classic + - 7 F/46 Ascending Hematochezia 1.8 NK Inflammatory ++ ++ 8 M/66 Ascending Abdominal pain 1.5 Yes Inflammatory ++ ++ 9 F/43 Descending None 0.5 No Sclerotic - - NK: Not Known The lesions in the first group (Fig. 1 , cases 1, 2, and 3) were classified as the early-stage type of IFP because of their relatively small sizes, with maximum diameters ranging from 0.2 to 0.3 cm. Microscopic examination revealed that two lesions were mostly located in the submucosa and exhibited only focal invasion of the lamina propria (Fig. 1 A, 1 F). In the third patient, the lesion invaded the lamina propria (Fig. 1 K), as evidenced by the rupture of the mucosal muscular layer (Fig. 1 O) and the reduced number of intrinsic glands. In two patients, the lesions consisted of thick-walled blood vessels (Fig. 1 B, 1 G). In all three cases, fibrosis deposition was observed around the blood vessels or between the glands, accompanied by minimal eosinophilic infiltration (Fig. 1 B, C, G, H, L, M). However, IHC staining revealed only a small number of CD34-positive cells in these lesions (Fig. 1 D, I, N), and PDGFRa was negative (Fig. 1 E). Masson staining confirmed the presence of fibrosis deposition (Fig. 1 J). The lesions in the second group (Fig. 2 , cases 4, 5, and 6) were identified as classic-type IFPs. Upon microscopic examination, we observed that these lesions extended from the submucosa into the lamina propria of the mucosa, resulting in a thinner or fractured mucosal muscular layer (Fig. 2 A, E) and a reduced number of intrinsic glands (Fig. 2 J). Thick-walled blood vessels were still present in the submucosa (Fig. 2 B). The characteristic "onion-skin-like" structure, composed of mild spindle-shaped cells surrounding the blood vessels or the glands, was present in these lesions (Fig. 2 B, G, K). Eosinophilic infiltration was observed in the "onion-skin-like" structure (Fig. 2 K). Notably, in one patient, we observed a dense arrangement of oval-shaped cells intermixed with adipocytes in a focal area (Fig. 2 F, case 5). Additionally, this patient exhibited significant infiltration of plasma cells (Fig. 2 G). IHC staining revealed that the "onion-skin-like" structures were negative (Fig. 2 C) or weakly positive (Fig. 2 L) for CD34 and negative for PDGFRa (Fig. 2 D, M). However, the densely arranged oval-shaped cells in case 5 were strongly positive for CD34 (Fig. 2 H) and weakly positive for PDGFRa (Fig. 2 I). The third group was inflammatory-type IFPs, which included two cases (Fig. 3 , case 7; Fig. 4 , case 8). They were significantly large, measuring at maximum diameters of 1.5 cm and 1.0 cm, respectively (Table 1 ). On the surface of the lesions, mucosal erosion was observed, accompanied by hyperplasia of granulation tissue (Fig. 3 A, 4 A). In the inner region of the lesions, spindle cells surrounding thick-walled and irregular blood vessels, along with significant infiltration of eosinophils, were observed (Fig. 3 B, 4 B). In the outer regions, there was notable infiltration of plasma cells between the glands (Fig. 3 C, 4 C). No residual mucosal muscular layer was detected in these two lesions. IHC staining revealed strong expression of CD34 in the central area of the lesions (Fig. 3 D, 3 E, 4 D, 4 E) but weaker expression in the peripheral regions (Fig. 3 F, 4 F). In contrast, PDGFRα was weakly expressed in the inner regions of the lesions (Fig. 3 G, 3 H, 4 G, 4 H) but was strongly expressed in the outer regions (Fig. 3 I, 4 I). The fourth group of IFPs, identified as the sclerotic type, was observed in case 9 (Fig. 5 ). The lesion was located in the submucosa (Fig. 5 A). The mucosamuscular layer appeared to be mostly intact, with slight thinning in focal areas (Fig. 5 B). Microscopic examination revealed numerous thick-walled blood vessels displaying hyaline degeneration. There was extensive collagen deposition between the blood vessels, along with mucinous degeneration (Fig. 5 C). Eosinophil infiltration was also observed in the focal areas of this lesion (Fig. 5 D). IHC staining indicated that both CD34 and PDGFRα were negative in this lesion (Fig. 5 E, F). Masson staining confirmed collagen deposition between the blood vessels (Fig. 5 G). Discussion In our retrospective analysis of data from the past seven years, we identified nine cases of IFP in the colon, three in the stomach, and two in the ileum. This means that colonic IFPs accounted for 60% of all IFP cases in the GI tract. These data significantly differ from previously reported findings. We believe that this discrepancy may be attributed to the high frequency of colorectal cancer screening conducted through microscopic examination, as mentioned in a previous study by Sánchez MM et al. ( 10 ). The typical pathological features of IFPs are characterized by an "onion-skin-like" morphology, as well as the expression of CD34, as determined by IHC staining ( 11 , 12 ). However, significant variations have been reported in both the histomorphology and immunophenotype of IFPs. For example, Y I Kim outlined the morphological changes in IFPs at different stages of progression ( 13 ). Ondrej Daum noted that CD34 is more likely to be positive in patients with an "onion-skin-like" appearance but more likely to be negative in patients with an “inflammatory pseudotumor-like” appearance ( 14 ). In this study, we also observed significant variations in both the morphology and immunoexpression features of colonic IFPs. On the basis of their clinicopathological features, we classified the nine cases of colonic IFPs into four groups. During endoscopy, three cases of early-stage type IFPs were incidentally discovered. These IFPs were all less than 0.5 cm in size and presented thick-walled blood vessels with minimal eosinophilic infiltration. However, they did not exhibit the characteristic "onion-skin-like" appearance. As a result, these IFPs may be classified as vascular malformations or other lesions with an indeterminate nature. Early-stage IFPs are notable for the presence of fibrosis around blood vessel walls. In our attempt to identify the underlying cause of this phenomenon, we found that two out of the three patients with early-stage-type IFPs also had type 2 diabetes. Previous research has suggested that diabetes can induce an inflammatory response in blood vessels, resulting in fibrinoid degeneration and eosinophilic infiltration ( 15 , 16 ). Therefore, our observations suggest that diabetes-induced fibrosis deposition may be an important factor in the development of IFP. The structural characteristics of classic-type IFPs in the colon are similar to those found in the stomach and small intestine. These features include a concentric, "onion-skin-like" appearance and varying levels of eosinophil infiltration. In the submucosa, thick-walled blood vessels were still present, providing evidence that classic-type IFPs may develop from early-stage IFPs. Notably, these lesions clearly extended from the submucosa into the lamina propria, as evidenced by the fractured or thinner mucosal muscular layer. This finding suggests that classic-type IFPs, even those that are small in size, are locally invasive. Unsurprisingly, as these lesions continue to grow, they may increase in size and present as more aggressive IFPs, as has been reported in the stomach and intestine ( 17 – 21 ). In this study, we also observed that classic IFPs may contain densely arranged oval cells mixed with mature adipocytes in a focal area. Additionally, we noted significant infiltration of plasma cells, which may be more prominent than eosinophilic infiltration. To the best of our knowledge, previous research has not noted this particular morphological feature in classic-type IFPs. Notably, the increase in cell density and infiltration of plasma cells may indicate the progression of this lesion. The two main methods for diagnosing IFP are IHC staining for CD34 and genetic testing for PDGFRα mutations. Research has shown that the majority (86%) of IFPs strongly express CD34 ( 22 ). However, our study revealed that classic type IFPs in the colon may exhibit weak positivity or even negativity for CD34. These findings indicate that the immunophenotypes of colonic IFPs may be atypical. The atypical expression of CD34 in colonic IFPs could cause confusion in diagnostic procedures, as CD34 is commonly used as a diagnostic marker for these lesions ( 23 ). On the other hand, the frequency of PDGFRα mutations in IFPs is estimated to be between 55.0% and 69.6% ( 9 ). Previous research has shown that 80% of IFPs with PDGFRα mutations also express PDGFRα, as determined by IHC staining. In contrast, IFPs without mutations in this gene do not express PDGFRα ( 24 , 25 ). In our study, through IHC staining, we found that all three classic types of IFPs in the colon do not express PDGFRα. These findings suggest that these IFPs do not have mutations in the PDGFRα gene. Schildhaus was the first to identify mutations in the PDGFRα gene in IFPs. However, upon reviewing his paper, we noted that this study included only one case of colonic IFP, which did not exhibit PDGFRα mutations ( 4 ). Therefore, we speculate that colonic IFPs, even those with classical morphological characteristics, may have a lower rate of PDGFRα gene mutations than gastric and small intestine IFPs. In future studies, we will collect additional cases of IFP and conduct gene mutation testing to validate our findings. In the inflammatory type of IFPs, we observed an "onion-skin-like" appearance in the inner region of these lesions, indicating that they may originate from classic type IFPs. However, this type of IFP is characterized by increased plasma cell infiltration surrounding the glands in the outer regions of the lesions. Interestingly, IHC staining revealed that CD34 is strongly expressed in the inner area of the lesions but weakly expressed in the outer regions. In contrast, PDGFRα is strongly expressed in the outer regions of lesions but weakly expressed in the inner region. These results suggest that the cells strongly positive for PDGFRα may be responsible for the aggregation of plasma cells in these lesions. PDGFRα is a member of the receptor tyrosine kinase family, and its signaling pathway plays a crucial role in the differentiation and growth of mesenchymal stem cells ( 26 , 27 ). Furthermore, PDGFRα signaling is essential for the aggregation of inflammatory cells, including plasma cells ( 28 ). On the basis of our findings, we hypothesize that CD34-positive mesenchymal stem cells in classic-type IFPs may acquire PDGFRα mutations, leading to their continued proliferation and the aggregation of plasma cells in these lesions. As a result, classic-type IFPs may gradually expand and eventually develop into the inflammatory type of IFPs. The sclerotic form of IFP has been reported by researchers, and it is believed to be in a spontaneously regressive stage because of significant collagen deposition within the lesion ( 13 ). In this study, we presented one case of the sclerotic type of IFP in the colon. Importantly, this lesion is located primarily in the submucosal areas, suggesting that it may originate from the degeneration of an early-stage type of IFP. Moreover, the sclerotic type of IFP may pose a challenge in pathological diagnosis, as it exhibits atypical morphology and is negative for CD34. Eosinophil infiltration in this lesion, however, may evoke memories of the diagnosis of IFP. On the basis of the morphological spectrum and immunoexpression of colonic IFPs, We have outlined that IFP may represent a group of diseases that start as non-neoplastic lesions (without PDGFR gene mutations), gradually evolve and acquire specific gene (PDGFR gene mutations) changes, and develop into true neoplastic lesions. We propose the following developmental pathways and outcomes. In the early stage, IFPs are confined to the submucosa and exhibit fibrosis deposition around blood vessels with minimal eosinophil infiltration. The lesion may become sclerotic due to the collagenization process of fibrosis deposition. Alternatively, the lesion may spread into the lamina propria of the mucosa and develop into the classic type of IFP. Notably, the early-stage type of IFP may not display PDGFRα gene mutations. The classic type of IFP has two distinct developmental outcomes as well. In some cases, CD34-positive mesenchymal stem cells acquire PDGFRα mutations. These cells then continuously proliferate and cause significant infiltration of plasma cells into the lesions. Ultimately, the classic type of IFP with PDGFRα mutations may develop into the inflammatory type of IFP. On the other hand, classic type IFP without PDGFRα mutation may spontaneously regress to the sclerotic type of IFP due to ongoing collagen deposition within the lesion. In this study, we present one case of the classic type of IFP that was weakly positive for PDGFRα, which may indicate the possibility of a PDGFRα gene mutation in this lesion. Moreover, we observed abundant plasma cell infiltration of the colonic IFP in this case (case 5). This observation indicating that this classic type of IFP with PDGFRα expression are developing into the inflammatory type of IFP, which may have verified our speculation about the outcome of the development of IFP. However, PDGFRα gene mutations were not detected directly in this patient. In the future, we plan to collect more cases of colonic IFP and conduct comprehensive molecular tests to further validate this hypothesis. Conclusions We presented the morphological spectrum and immunoexpression features of four groups of colonic IFPs and outlined the potential developmental outcomes of these lesions. We remind readers that IFPs in the colon, even when displaying the characteristic appearance, may exhibit weak or negative IHC staining for both CD34 and PDGFRα. We propose that only inflammatory-type and classic-type IFPs with PDGFRα mutations or immunoexpression have the potential for continued growth. These lesions should be regarded as genuine neoplastic lesions. This study significantly enhances our understanding of the pathological characteristics of colonic IFPs and provides valuable insights for their diagnosis. Declarations 1. Ethics approval and consent to participate The study protocol was approved by the Institutional Review Board of the Seventh Affiliated Hospital of Sun Yat-sen University. 2. Consent for publication Not applicable 3. Availability of data and materials Not applicable. 4. Competing interests None 5. Funding No funding was involved in this study 6. Authors' contributions QCF: Literature search, study design and concept drafting, references and writing of manuscript. LXL and ZTZ: Literature search, study design, writing of manuscript and interpretation of results. LDZ and WZ: IHC staining and review of final manuscript. 7. Acknowledgement None References Vanek J. Gastric submucosal granuloma with eosinophilic infiltration. The American journal of pathology. 1949;25(3):397-411. Helwig EB, Ranier A. Inflammatory fibroid polyps of the stomach. Surgery, gynecology & obstetrics. 1953;96(3):335-67. Schildhaus HU, Merkelbach-Bruse S, Binot E, Büttner R, Wardelmann E. 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Cite Share Download PDF Status: Published Journal Publication published 23 Oct, 2025 Read the published version in Diagnostic Pathology → Version 1 posted Editorial decision: Revision requested 03 Sep, 2025 Reviews received at journal 03 Sep, 2025 Reviewers agreed at journal 03 Sep, 2025 Reviewers invited by journal 02 Sep, 2025 Submission checks completed at journal 02 Sep, 2025 First submitted to journal 01 Sep, 2025 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-7257229","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":509188917,"identity":"059ce053-fbb7-4af7-86a8-5f52d7bbd482","order_by":0,"name":"Qin Changfei","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAABAUlEQVRIiWNgGAWjYDACZhCyqZFjYGBsPAATlCCsJe2YMVBLA5FawLrSmBMbgAzitPAd5z34uSCBLX1t+2GgLX8O2xscYD54m4fBLg+XFsnDfMnSMxJkcredSWw4wNh2OHHDAbZkax6G5GJcWgwO85gx8/5gy912AKSl4XCCwQEeM2kehgNgp+LUwpPAnG52/iHMYfzfiNKSYHYDaAsD22HGDQd42PBqkTzMYyzNk3DMcNsNoC2JbemJMw+zGVvOMUjGqYXv/BnDzzwJNfJm59MfPvjwx9qe73jzwxtvKuxwakHEBQgkMDSDIxfoYFzq0bUwMNThUToKRsEoGAUjFQAA23VaGGHAoQoAAAAASUVORK5CYII=","orcid":"","institution":"the Seventh Affiliated Hospital of Sun Yat-sen University","correspondingAuthor":true,"prefix":"","firstName":"Qin","middleName":"","lastName":"Changfei","suffix":""},{"id":509188918,"identity":"41c27e22-175c-4e12-9ff4-0b4d39c24a11","order_by":1,"name":"Zhang Tingzhen","email":"","orcid":"","institution":"the Seventh Affiliated Hospital of Sun Yat-sen University","correspondingAuthor":false,"prefix":"","firstName":"Zhang","middleName":"","lastName":"Tingzhen","suffix":""},{"id":509188919,"identity":"6cf844f2-537f-44a4-91b5-2cb649394fda","order_by":2,"name":"Lin Xiangling","email":"","orcid":"","institution":"the Seventh Affiliated Hospital of Sun Yat-sen University","correspondingAuthor":false,"prefix":"","firstName":"Lin","middleName":"","lastName":"Xiangling","suffix":""},{"id":509188920,"identity":"2577d4d5-b901-456f-a94a-598511e767f9","order_by":3,"name":"Liao Dingzhun","email":"","orcid":"","institution":"the Seventh Affiliated Hospital of Sun Yat-sen University","correspondingAuthor":false,"prefix":"","firstName":"Liao","middleName":"","lastName":"Dingzhun","suffix":""},{"id":509188921,"identity":"455f0c18-865b-4c0d-be87-a1e02a35bf0b","order_by":4,"name":"Wen Zhang","email":"","orcid":"","institution":"the Seventh Affiliated Hospital of Sun Yat-sen University","correspondingAuthor":false,"prefix":"","firstName":"Wen","middleName":"","lastName":"Zhang","suffix":""}],"badges":[],"createdAt":"2025-07-31 02:23:21","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-7257229/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-7257229/v1","draftVersion":[],"editorialEvents":[{"content":"https://doi.org/10.1186/s13000-025-01722-2","type":"published","date":"2025-10-23T16:17:22+00:00"}],"editorialNote":"","failedWorkflow":false,"files":[{"id":90791034,"identity":"a27f2c71-954a-4b49-ac2c-c2d13862e112","added_by":"auto","created_at":"2025-09-08 08:19:26","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":1890078,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eEarly-stage IFPs in the colon.\u003c/strong\u003eIn Patient 1 (A-E), the lesion was located in the submucosa (A) and consisted of thick-walled blood vessels (B). Fibrosis deposition around the blood vessels was accompanied by a small amount of eosinophilic infiltration (C). CD34 was expressed in very few cells (D), and PDGFRα was negative (E). In Patient 2 (F-J), the lesion showed focal invasion into the lamina propria (F). Fibrosis deposition was observed around the blood vessels (G) and between the glands (H). Only a small number of cells expressed CD34 (I). Masson staining confirmed the presence of fibrosis (J). In Patient 3 (K-O), the lesion had invaded the lamina propria (K). Fibrosis deposition was evident around the blood vessels (L) and between the glands (M). There were very few CD34-positive cells (N). IHC staining of the SMA revealed a fractured mucosal muscular layer (O).\u003c/p\u003e","description":"","filename":"floatimage1.png","url":"https://assets-eu.researchsquare.com/files/rs-7257229/v1/6b8c542725bae2a185209bf7.png"},{"id":90791032,"identity":"b342618d-90a6-4feb-b148-5af43d02ecbe","added_by":"auto","created_at":"2025-09-08 08:19:26","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":1699819,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eThe classical type of IFPs in the colon.\u003c/strong\u003eIn Patient 4 (A-D), the lesion extended into the lamina propria, resulting in a thinner mucosal muscular layer (A). Thick-walled blood vessels were still visible in the submucosa (B). The \"onion-skin-like\" structure was negative for both CD34 (C) and PDGFRα (D). In Patient 5 (E-I), the lesion broke through the mucosal muscular layer, resulting in a fractured mucosal muscular layer (E). The lesion consisted of densely arranged oval-shaped cells intermixed with mature adipocytes in a focal area (F). There was a significant number of plasma cells (G). The oval-shaped cells were strongly positive for CD34 (H) and weakly positive for PDGFRα (I). In Patient 6 (J-M), the intrinsic glands in the lamina propria were significantly reduced (J). The characteristic \"onion-skin-like\" appearance (K) was weakly positive for CD34 (L) and negative for PDGFRα (M).\u003c/p\u003e","description":"","filename":"floatimage2.png","url":"https://assets-eu.researchsquare.com/files/rs-7257229/v1/26280dc2556b787f4d69f8b0.png"},{"id":90792334,"identity":"95a370ad-9afd-4d55-9943-30ae767247e9","added_by":"auto","created_at":"2025-09-08 08:27:26","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":1774771,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eThe inflammatory type of IFP in the colon.\u003c/strong\u003eIn Patient 7, the lesion was a polypoid mass with mucosal erosion on the surface (A). The inner region was characterized by spindle cells surrounding thick-walled blood vessels, with a significant number of eosinophils infiltrating (B). In the outer regions, there was significant infiltration of plasma cells between the glands (C). CD34 was strongly expressed in the inner area of the lesion but only weakly expressed in the outer regions (D-F). PDGFRα was strongly expressed in the outer region of the lesion but weakly expressed in the inner region (G-I).\u003c/p\u003e","description":"","filename":"floatimage3.png","url":"https://assets-eu.researchsquare.com/files/rs-7257229/v1/1f41281575e3670d95115036.png"},{"id":90791052,"identity":"3321773d-4851-4918-84bb-d4505abe5afe","added_by":"auto","created_at":"2025-09-08 08:19:27","extension":"png","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":1825762,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eThe inflammatory type of IFP in the colon.\u003c/strong\u003eIn Patient 8, the lesion was a polypoid mass with mucosal erosion on the surface (A). The inner region was characterized by spindle cells surrounding thick-walled blood vessels, along with significant infiltration of eosinophils (B). In the outer region, there was an aggregation of plasma cells between the glands (C). CD34 was strongly expressed in the inner area of the lesion but only weakly expressed in the outer regions (D-F). PDGFRα was strongly expressed in the outer region of the lesion but weakly expressed in the inner region (G-I).\u003c/p\u003e","description":"","filename":"floatimage4.png","url":"https://assets-eu.researchsquare.com/files/rs-7257229/v1/cfc7e49fd261d768c51f44e8.png"},{"id":90791051,"identity":"f32663b3-76cd-4ccc-8d24-8588f524ab3f","added_by":"auto","created_at":"2025-09-08 08:19:26","extension":"png","order_by":5,"title":"Figure 5","display":"","copyAsset":false,"role":"figure","size":1258886,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eThe sclerotic type of IFP in the colon.\u003c/strong\u003eIn Patient 9, the lesion was located in the submucosa (A). The mucosal muscular layer appeared to be slightly thinner in focal areas (B). This lesion consisted of thick-walled blood vessels displaying glassy degeneration, considerable collagen deposition and mucinous degeneration (C). Eosinophil infiltration was observed in focal areas (D). The lesion was negative for CD34 (E) and PDGFRα (F). Masson staining confirmed the presence of collagen deposition (G).\u003c/p\u003e","description":"","filename":"floatimage5.png","url":"https://assets-eu.researchsquare.com/files/rs-7257229/v1/63a6559111dd9f87adf885cd.png"},{"id":94490418,"identity":"2bf150c2-b150-402c-8221-b8bd2454bff9","added_by":"auto","created_at":"2025-10-27 17:09:55","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":9967651,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-7257229/v1/9b931a39-f066-4ced-bc1b-6842142cad3d.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Inflammatory Fibroid Polyps of the Colon: A Study on the Morphological Spectrum, Immunoexpression Characteristics, and Outcomes","fulltext":[{"header":"Introduction","content":"\u003cp\u003eIn 1949, Vanek first reported six cases of polypoid lesions in the stomach. He described them as submucosal granulomas with eosinophilic infiltration, on the basis of their morphological features (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). In 1953, Helwig and Ranier introduced the term inflammatory fibrous polyp (IFP) to describe these lesions, a term that has become widely used and accepted (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e, \u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e). In a groundbreaking study in 2008, Schildhaus et al. demonstrated that the majority of IFPs possess mutations in the platelet-derived growth factor receptor alpha (PDGFRα) gene, providing evidence that IFPs are genuine neoplastic lesions (\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e). As a result, both the fourth edition in 2010 and the fifth edition in 2019 of the World Health Organization's Classification of Tumors of the Digestive System classified IFPs as benign mesenchymal tumors of the digestive system (\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eIFPs can develop anywhere in the gastrointestinal (GI) tract. They are most commonly found in the stomach (66.7%) and the small intestine (21.1%), as reported previously (\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e). Research has shown that the morphological and genetic features of IFPs vary depending on their location in the body. For example, gastric IFPs often exhibit characteristic \"onion skin-like\" structures, with spindle-shaped or oval-shaped tumor cells arranged in a vortex pattern around blood vessels or mucosal glands. This is often accompanied by the infiltration of eosinophils. In contrast, IFPs in the small intestine typically present a significant presence of mixed inflammatory cells, including eosinophils, lymphocytes, plasma cells, and mast cells. However, the \"onion skin-like\" structure is uncommon in this location (\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e). Furthermore, 53.3% of gastric IFPs carry a PDGFRα gene mutation, with most (68.8%) mutations located in exon 18. In comparison, 58.0% of IFPs in the small intestine carry a mutation in this gene, with the majority (83.0%) of mutations located in exon 12 (\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e).\u003c/p\u003e\u003cp\u003ePrevious studies have shown that the colon is a rare site for IFP, accounting for only 8.4% of all cases (\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e). However, in our practical experience, we have observed a greater prevalence of IFP in the colon than in the gastric and small intestine. This study presents nine cases of colonic IFP at various stages of progression, providing a comprehensive overview of the morphological spectrum and immunoexpression characteristics of this lesion. Our findings indicate that only the inflammatory type of IFPs, along with a subset of classic type IFPs exhibiting PDGFRα gene mutations, have the potential for continued growth.\u003c/p\u003e"},{"header":"Materials and methods","content":"\u003cp\u003eNine cases of colonic IFPs collected between 2014 and 2020 were retrieved from the files of the Department of Pathology at Sun Yat-sen University Seventh Affiliated Hospital. Clinical data for all patients were collected. At least two pathologists reviewed the pathological sections to confirm the diagnosis.\u003c/p\u003e\u003cp\u003eThe samples were fixed in 4% formaldehyde and embedded in paraffin via standard procedures. Sections measuring 3\u0026ndash;4 \u0026micro;m were cut from the tissue blocks and stained with hematoxylin‒eosin (H\u0026amp;E). For immunohistochemical (IHC) staining, the EnVision two-step method was employed. Antigen retrieval was conducted at high temperature. The following primary antibodies were used: CD34 (DAKO, QBEnd 10), CD117 (Roche, 9.7), Desmin (ZSGB-BIO, OTIR4A8), DOG-1 (MXB, SP31), Ki-67 (DAKO, MIB-1), PDGFRα (ZSGB-BIO, ZA-0377), SMA (DAKO, 1A4), and S-100 (DAKO, ZO311). Both positive and negative controls are shown on the slides. Immunopositivity was described as negative (-), focal positive (+) when less than 50% of the cells exhibited staining, and positive (++) when more than 50% of the cells showed staining. H\u0026amp;E- and IHC-stained sections were scanned via the MagScanner (KF-PRO-005). Typical pathological images were captured from the scanned sections.\u003c/p\u003e"},{"header":"Results","content":"\u003cp\u003eTable\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e provides a comprehensive summary of the clinicopathological characteristics of the nine patients with colonic IFPs. Among the nine patients, three were diagnosed with male patients, and six were diagnosed with female patients, resulting in a male-to-female ratio of 1:2. The age range of the patients was 35\u0026ndash;66 years, with a median age of 43 years. Four cases were located in the ascending colon, two in the transverse colon, and three in the descending or sigmoid colon. Four patients experienced symptoms such as diarrhea, hematochezia, and abdominal pain. In two patients, endoscopic findings revealed a polypoid mass in the intestinal lumen, whereas the remaining seven patients presented with sessile lesions. Notably, five out of the nine patients had type 2 diabetes. IHC staining for CD117, DOG-1, Desmin, SMA, and S-100 was performed to exclude differential diagnoses, including gastrointestinal stromal tumors (GISTs), smooth muscle tumors, inflammatory myofibroblastic tumors (IMTs), and neural tumors, respectively. These nine cases of colonic IFP can be classified into four types on the basis of their pathological features.\u003c/p\u003e\u003cp\u003e\u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e\u003ccaption language=\"En\"\u003e\u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e\u003cdiv class=\"CaptionContent\"\u003e\u003cp\u003eClinicopathological (histological \u0026amp; immunohistochemical) features of colonic IFP.\u003c/p\u003e\u003c/div\u003e\u003c/caption\u003e\u003ccolgroup cols=\"9\"\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e\u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c6\" colnum=\"6\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c7\" colnum=\"7\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c8\" colnum=\"8\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c9\" colnum=\"9\"\u003e\u003c/div\u003e\u003cthead\u003e\u003ctr\u003e\u003cth align=\"left\" colname=\"c1\" morerows=\"1\" rowspan=\"2\"\u003e\u003cp\u003eCase\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c2\" morerows=\"1\" rowspan=\"2\"\u003e\u003cp\u003eSex/age\u003c/p\u003e\u003cp\u003e(years)\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c3\" morerows=\"1\" rowspan=\"2\"\u003e\u003cp\u003eLocation(colon)\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c4\" morerows=\"1\" rowspan=\"2\"\u003e\u003cp\u003eSymptom\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c5\" morerows=\"1\" rowspan=\"2\"\u003e\u003cp\u003eSize (cm)\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c6\" morerows=\"1\" rowspan=\"2\"\u003e\u003cp\u003eDiabetes\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c7\" morerows=\"1\" rowspan=\"2\"\u003e\u003cp\u003eHistologic type\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colspan=\"2\" nameend=\"c9\" namest=\"c8\"\u003e\u003cp\u003eIHC\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003ctr\u003e\u003cth align=\"left\" colname=\"c8\"\u003e\u003cp\u003eCD34\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c9\"\u003e\u003cp\u003ePDGFRα\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003c/thead\u003e\u003ctbody\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e1\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eF/44\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" 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colname=\"c5\"\u003e\u003cp\u003e0.3\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003eYes\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003eEarly-stage\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c8\"\u003e\u003cp\u003e+\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c9\"\u003e\u003cp\u003e-\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e4\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eF/39\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eTransverse\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003eDiarrhea\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e\u003cp\u003e0.4\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003eNK\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003eClassic\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c8\"\u003e\u003cp\u003e-\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c9\"\u003e\u003cp\u003e-\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e5\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eM/44\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eSigmoid\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003eNone\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e\u003cp\u003e0.5\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003eYes\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003eClassic\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c8\"\u003e\u003cp\u003e++\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c9\"\u003e\u003cp\u003e+\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e6\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eF/42\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eTransverse\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003eNone\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e\u003cp\u003e0.6\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003eNo\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003eClassic\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c8\"\u003e\u003cp\u003e+\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c9\"\u003e\u003cp\u003e-\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e7\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eF/46\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eAscending\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003eHematochezia\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e\u003cp\u003e1.8\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003eNK\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003eInflammatory\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c8\"\u003e\u003cp\u003e++\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c9\"\u003e\u003cp\u003e++\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e8\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eM/66\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eAscending\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003eAbdominal pain\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e\u003cp\u003e1.5\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003eYes\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003eInflammatory\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c8\"\u003e\u003cp\u003e++\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c9\"\u003e\u003cp\u003e++\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e9\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eF/43\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eDescending\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003eNone\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e\u003cp\u003e0.5\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003eNo\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003eSclerotic\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c8\"\u003e\u003cp\u003e-\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c9\"\u003e\u003cp\u003e-\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003c/tbody\u003e\u003c/colgroup\u003e\u003ctfoot\u003e\u003ctr\u003e\u003ctd colspan=\"9\"\u003e\u003cb\u003eNK: Not Known\u003c/b\u003e\u003c/td\u003e\u003c/tr\u003e\u003c/tfoot\u003e\u003c/table\u003e\u003c/div\u003e\u003c/p\u003e\u003cp\u003eThe lesions in the first group (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e, cases 1, 2, and 3) were classified as the early-stage type of IFP because of their relatively small sizes, with maximum diameters ranging from 0.2 to 0.3 cm. Microscopic examination revealed that two lesions were mostly located in the submucosa and exhibited only focal invasion of the lamina propria (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eA, \u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eF). In the third patient, the lesion invaded the lamina propria (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eK), as evidenced by the rupture of the mucosal muscular layer (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eO) and the reduced number of intrinsic glands. In two patients, the lesions consisted of thick-walled blood vessels (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eB, \u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eG). In all three cases, fibrosis deposition was observed around the blood vessels or between the glands, accompanied by minimal eosinophilic infiltration (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eB, C, G, H, L, M). However, IHC staining revealed only a small number of CD34-positive cells in these lesions (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eD, I, N), and PDGFRa was negative (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eE). Masson staining confirmed the presence of fibrosis deposition (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eJ).\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003cp\u003eThe lesions in the second group (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e, cases 4, 5, and 6) were identified as classic-type IFPs. Upon microscopic examination, we observed that these lesions extended from the submucosa into the lamina propria of the mucosa, resulting in a thinner or fractured mucosal muscular layer (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003eA, E) and a reduced number of intrinsic glands (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003eJ). Thick-walled blood vessels were still present in the submucosa (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003eB). The characteristic \"onion-skin-like\" structure, composed of mild spindle-shaped cells surrounding the blood vessels or the glands, was present in these lesions (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003eB, G, K). Eosinophilic infiltration was observed in the \"onion-skin-like\" structure (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003eK). Notably, in one patient, we observed a dense arrangement of oval-shaped cells intermixed with adipocytes in a focal area (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003eF, case 5). Additionally, this patient exhibited significant infiltration of plasma cells (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003eG). IHC staining revealed that the \"onion-skin-like\" structures were negative (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003eC) or weakly positive (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003eL) for CD34 and negative for PDGFRa (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003eD, M). However, the densely arranged oval-shaped cells in case 5 were strongly positive for CD34 (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003eH) and weakly positive for PDGFRa (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003eI).\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003cp\u003eThe third group was inflammatory-type IFPs, which included two cases (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003e, case 7; Fig.\u0026nbsp;\u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003e, case 8). They were significantly large, measuring at maximum diameters of 1.5 cm and 1.0 cm, respectively (Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). On the surface of the lesions, mucosal erosion was observed, accompanied by hyperplasia of granulation tissue (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003eA, \u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003eA). In the inner region of the lesions, spindle cells surrounding thick-walled and irregular blood vessels, along with significant infiltration of eosinophils, were observed (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003eB, \u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003eB). In the outer regions, there was notable infiltration of plasma cells between the glands (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003eC, \u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003eC). No residual mucosal muscular layer was detected in these two lesions. IHC staining revealed strong expression of CD34 in the central area of the lesions (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003eD, \u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003eE, \u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003eD, \u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003eE) but weaker expression in the peripheral regions (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003eF, \u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003eF). In contrast, PDGFRα was weakly expressed in the inner regions of the lesions (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003eG, \u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003eH, \u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003eG, \u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003eH) but was strongly expressed in the outer regions (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003eI, \u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003eI).\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003cp\u003eThe fourth group of IFPs, identified as the sclerotic type, was observed in case 9 (Fig.\u0026nbsp;\u003cspan refid=\"Fig5\" class=\"InternalRef\"\u003e5\u003c/span\u003e). The lesion was located in the submucosa (Fig.\u0026nbsp;\u003cspan refid=\"Fig5\" class=\"InternalRef\"\u003e5\u003c/span\u003eA). The mucosamuscular layer appeared to be mostly intact, with slight thinning in focal areas (Fig.\u0026nbsp;\u003cspan refid=\"Fig5\" class=\"InternalRef\"\u003e5\u003c/span\u003eB). Microscopic examination revealed numerous thick-walled blood vessels displaying hyaline degeneration. There was extensive collagen deposition between the blood vessels, along with mucinous degeneration (Fig.\u0026nbsp;\u003cspan refid=\"Fig5\" class=\"InternalRef\"\u003e5\u003c/span\u003eC). Eosinophil infiltration was also observed in the focal areas of this lesion (Fig.\u0026nbsp;\u003cspan refid=\"Fig5\" class=\"InternalRef\"\u003e5\u003c/span\u003eD). IHC staining indicated that both CD34 and PDGFRα were negative in this lesion (Fig.\u0026nbsp;\u003cspan refid=\"Fig5\" class=\"InternalRef\"\u003e5\u003c/span\u003eE, F). Masson staining confirmed collagen deposition between the blood vessels (Fig.\u0026nbsp;\u003cspan refid=\"Fig5\" class=\"InternalRef\"\u003e5\u003c/span\u003eG).\u003c/p\u003e\u003cp\u003e\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eIn our retrospective analysis of data from the past seven years, we identified nine cases of IFP in the colon, three in the stomach, and two in the ileum. This means that colonic IFPs accounted for 60% of all IFP cases in the GI tract. These data significantly differ from previously reported findings. We believe that this discrepancy may be attributed to the high frequency of colorectal cancer screening conducted through microscopic examination, as mentioned in a previous study by S\u0026aacute;nchez MM et al. (\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e). The typical pathological features of IFPs are characterized by an \"onion-skin-like\" morphology, as well as the expression of CD34, as determined by IHC staining (\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e, \u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e). However, significant variations have been reported in both the histomorphology and immunophenotype of IFPs. For example, Y I Kim outlined the morphological changes in IFPs at different stages of progression (\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e). Ondrej Daum noted that CD34 is more likely to be positive in patients with an \"onion-skin-like\" appearance but more likely to be negative in patients with an \u0026ldquo;inflammatory pseudotumor-like\u0026rdquo; appearance (\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e). In this study, we also observed significant variations in both the morphology and immunoexpression features of colonic IFPs. On the basis of their clinicopathological features, we classified the nine cases of colonic IFPs into four groups.\u003c/p\u003e\u003cp\u003eDuring endoscopy, three cases of early-stage type IFPs were incidentally discovered. These IFPs were all less than 0.5 cm in size and presented thick-walled blood vessels with minimal eosinophilic infiltration. However, they did not exhibit the characteristic \"onion-skin-like\" appearance. As a result, these IFPs may be classified as vascular malformations or other lesions with an indeterminate nature. Early-stage IFPs are notable for the presence of fibrosis around blood vessel walls. In our attempt to identify the underlying cause of this phenomenon, we found that two out of the three patients with early-stage-type IFPs also had type 2 diabetes. Previous research has suggested that diabetes can induce an inflammatory response in blood vessels, resulting in fibrinoid degeneration and eosinophilic infiltration (\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e, \u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e). Therefore, our observations suggest that diabetes-induced fibrosis deposition may be an important factor in the development of IFP.\u003c/p\u003e\u003cp\u003eThe structural characteristics of classic-type IFPs in the colon are similar to those found in the stomach and small intestine. These features include a concentric, \"onion-skin-like\" appearance and varying levels of eosinophil infiltration. In the submucosa, thick-walled blood vessels were still present, providing evidence that classic-type IFPs may develop from early-stage IFPs. Notably, these lesions clearly extended from the submucosa into the lamina propria, as evidenced by the fractured or thinner mucosal muscular layer. This finding suggests that classic-type IFPs, even those that are small in size, are locally invasive. Unsurprisingly, as these lesions continue to grow, they may increase in size and present as more aggressive IFPs, as has been reported in the stomach and intestine (\u003cspan additionalcitationids=\"CR18 CR19 CR20\" citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e). In this study, we also observed that classic IFPs may contain densely arranged oval cells mixed with mature adipocytes in a focal area. Additionally, we noted significant infiltration of plasma cells, which may be more prominent than eosinophilic infiltration. To the best of our knowledge, previous research has not noted this particular morphological feature in classic-type IFPs. Notably, the increase in cell density and infiltration of plasma cells may indicate the progression of this lesion.\u003c/p\u003e\u003cp\u003eThe two main methods for diagnosing IFP are IHC staining for CD34 and genetic testing for PDGFRα mutations. Research has shown that the majority (86%) of IFPs strongly express CD34 (\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e). However, our study revealed that classic type IFPs in the colon may exhibit weak positivity or even negativity for CD34. These findings indicate that the immunophenotypes of colonic IFPs may be atypical. The atypical expression of CD34 in colonic IFPs could cause confusion in diagnostic procedures, as CD34 is commonly used as a diagnostic marker for these lesions (\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e). On the other hand, the frequency of PDGFRα mutations in IFPs is estimated to be between 55.0% and 69.6% (\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e). Previous research has shown that 80% of IFPs with PDGFRα mutations also express PDGFRα, as determined by IHC staining. In contrast, IFPs without mutations in this gene do not express PDGFRα (\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e, \u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e). In our study, through IHC staining, we found that all three classic types of IFPs in the colon do not express PDGFRα. These findings suggest that these IFPs do not have mutations in the PDGFRα gene. Schildhaus was the first to identify mutations in the PDGFRα gene in IFPs. However, upon reviewing his paper, we noted that this study included only one case of colonic IFP, which did not exhibit PDGFRα mutations (\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e). Therefore, we speculate that colonic IFPs, even those with classical morphological characteristics, may have a lower rate of PDGFRα gene mutations than gastric and small intestine IFPs. In future studies, we will collect additional cases of IFP and conduct gene mutation testing to validate our findings.\u003c/p\u003e\u003cp\u003eIn the inflammatory type of IFPs, we observed an \"onion-skin-like\" appearance in the inner region of these lesions, indicating that they may originate from classic type IFPs. However, this type of IFP is characterized by increased plasma cell infiltration surrounding the glands in the outer regions of the lesions. Interestingly, IHC staining revealed that CD34 is strongly expressed in the inner area of the lesions but weakly expressed in the outer regions. In contrast, PDGFRα is strongly expressed in the outer regions of lesions but weakly expressed in the inner region. These results suggest that the cells strongly positive for PDGFRα may be responsible for the aggregation of plasma cells in these lesions. PDGFRα is a member of the receptor tyrosine kinase family, and its signaling pathway plays a crucial role in the differentiation and growth of mesenchymal stem cells (\u003cspan citationid=\"CR26\" class=\"CitationRef\"\u003e26\u003c/span\u003e, \u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e27\u003c/span\u003e). Furthermore, PDGFRα signaling is essential for the aggregation of inflammatory cells, including plasma cells (\u003cspan citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e). On the basis of our findings, we hypothesize that CD34-positive mesenchymal stem cells in classic-type IFPs may acquire PDGFRα mutations, leading to their continued proliferation and the aggregation of plasma cells in these lesions. As a result, classic-type IFPs may gradually expand and eventually develop into the inflammatory type of IFPs.\u003c/p\u003e\u003cp\u003eThe sclerotic form of IFP has been reported by researchers, and it is believed to be in a spontaneously regressive stage because of significant collagen deposition within the lesion (\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e). In this study, we presented one case of the sclerotic type of IFP in the colon. Importantly, this lesion is located primarily in the submucosal areas, suggesting that it may originate from the degeneration of an early-stage type of IFP. Moreover, the sclerotic type of IFP may pose a challenge in pathological diagnosis, as it exhibits atypical morphology and is negative for CD34. Eosinophil infiltration in this lesion, however, may evoke memories of the diagnosis of IFP.\u003c/p\u003e\u003cp\u003eOn the basis of the morphological spectrum and immunoexpression of colonic IFPs, We have outlined that IFP may represent a group of diseases that start as non-neoplastic lesions (without PDGFR gene mutations), gradually evolve and acquire specific gene (PDGFR gene mutations) changes, and develop into true neoplastic lesions. We propose the following developmental pathways and outcomes. In the early stage, IFPs are confined to the submucosa and exhibit fibrosis deposition around blood vessels with minimal eosinophil infiltration. The lesion may become sclerotic due to the collagenization process of fibrosis deposition. Alternatively, the lesion may spread into the lamina propria of the mucosa and develop into the classic type of IFP. Notably, the early-stage type of IFP may not display PDGFRα gene mutations. The classic type of IFP has two distinct developmental outcomes as well. In some cases, CD34-positive mesenchymal stem cells acquire PDGFRα mutations. These cells then continuously proliferate and cause significant infiltration of plasma cells into the lesions. Ultimately, the classic type of IFP with PDGFRα mutations may develop into the inflammatory type of IFP. On the other hand, classic type IFP without PDGFRα mutation may spontaneously regress to the sclerotic type of IFP due to ongoing collagen deposition within the lesion.\u003c/p\u003e\u003cp\u003eIn this study, we present one case of the classic type of IFP that was weakly positive for PDGFRα, which may indicate the possibility of a PDGFRα gene mutation in this lesion. Moreover, we observed abundant plasma cell infiltration of the colonic IFP in this case (case 5). This observation indicating that this classic type of IFP with PDGFRα expression are developing into the inflammatory type of IFP, which may have verified our speculation about the outcome of the development of IFP. However, PDGFRα gene mutations were not detected directly in this patient. In the future, we plan to collect more cases of colonic IFP and conduct comprehensive molecular tests to further validate this hypothesis.\u003c/p\u003e"},{"header":"Conclusions","content":"\u003cp\u003eWe presented the morphological spectrum and immunoexpression features of four groups of colonic IFPs and outlined the potential developmental outcomes of these lesions. We remind readers that IFPs in the colon, even when displaying the characteristic appearance, may exhibit weak or negative IHC staining for both CD34 and PDGFRα. We propose that only inflammatory-type and classic-type IFPs with PDGFRα mutations or immunoexpression have the potential for continued growth. These lesions should be regarded as genuine neoplastic lesions. This study significantly enhances our understanding of the pathological characteristics of colonic IFPs and provides valuable insights for their diagnosis.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003e1. Ethics approval and consent to participate\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe study protocol was approved by the Institutional Review Board of the Seventh Affiliated Hospital of Sun Yat-sen University.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e2. Consent for publication\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e3. Availability of data and materials\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e4. Competing interests\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNone\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e5. Funding\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNo funding was involved in this study\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e6. Authors\u0026apos; contributions\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eQCF: Literature search, study design and concept drafting, references and writing of manuscript.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eLXL and ZTZ: Literature search, study design, writing of manuscript and interpretation of results.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eLDZ and WZ: IHC staining and review of final manuscript.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e7. Acknowledgement\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNone \u0026nbsp;\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eVanek J. Gastric submucosal granuloma with eosinophilic infiltration. The American journal of pathology. 1949;25(3):397-411.\u003c/li\u003e\n\u003cli\u003eHelwig EB, Ranier A. Inflammatory fibroid polyps of the stomach. Surgery, gynecology \u0026amp; obstetrics. 1953;96(3):335-67.\u003c/li\u003e\n\u003cli\u003eSchildhaus HU, Merkelbach-Bruse S, Binot E, B\u0026uuml;ttner R, Wardelmann E. [Inflammatory fibroid polyp: from Vanek\u0026apos;s \u0026quot;submucosal granuloma\u0026quot; to the concept of submucosal mesenchymal neoplasia]. Der Pathologe. 2010;31(2):109-14.\u003c/li\u003e\n\u003cli\u003eSchildhaus HU, Cavlar T, Binot E, B\u0026uuml;ttner R, Wardelmann E, Merkelbach-Bruse S. Inflammatory fibroid polyps harbour mutations in the platelet-derived growth factor receptor alpha (PDGFRA) gene. 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International immunology. 2018;30(6):241-53.\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":true,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"diagnostic-pathology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"dpat","sideBox":"Learn more about [Diagnostic Pathology](http://diagnosticpathology.biomedcentral.com)","snPcode":"13000","submissionUrl":"https://submission.nature.com/new-submission/13000/3","title":"Diagnostic Pathology","twitterHandle":"@OncoBioMed","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"em","reportingPortfolio":"BMC/SO AJ","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Inflammatory Fibrous Polyp, Colon, Morphological Spectrum, Immunoexpression, Outcome","lastPublishedDoi":"10.21203/rs.3.rs-7257229/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-7257229/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eBackground: \u003c/strong\u003eColonic inflammatory fibroid polyps (IFPs) have not been extensively studied.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eMethods:\u003c/strong\u003e In this study, We collected nine cases of colonic IFPs and provide a comprehensive description of the clinicopathological features and developmental outcomes of these lesions.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eResults: \u003c/strong\u003eThese nine cases of colonic IFPs can be classified into four types on the basis of their pathological characteristics: early-stage, classic, inflammatory, and sclerotic. The early-stage type of IFP is characterized by the deposition of fibrosis around blood vessels and between glands. The classic type of IFP is easily identifiable by its \"onion-skin-like\" structure; however, immunohistochemical (IHC) staining for CD34 may demonstrate focal positivity or even negativity. The inflammatory type of IFP is large and characterized by significant infiltration of plasma cells. IHC staining revealed variable positivity for both CD34 and PDGFRα across different regions of the lesions. The sclerotic type of IFP is characterized by substantial deposition of collagen. Furthermore, our findings suggest that early-stage IFPs have the potential to either develop into classic-type IFPs or degenerate into sclerotic-type IFPs. Additionally, classic-type IFPs may acquire PDGFRα mutations and ultimately transform into inflammatory-type IFPs.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusions: \u003c/strong\u003eColonic IFPs exhibit a distinct morphological spectrum and unique immunoexpressioncharacteristics as they progress. Only inflammatory-type and classic-type IFPs with PDGFRα mutations or immunoexpression should be regarded as genuine neoplastic lesions.\u003c/p\u003e","manuscriptTitle":"Inflammatory Fibroid Polyps of the Colon: A Study on the Morphological Spectrum, Immunoexpression Characteristics, and Outcomes","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-09-08 08:19:21","doi":"10.21203/rs.3.rs-7257229/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2025-09-03T23:58:39+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-09-03T13:45:21+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"193241862179789115986730793192160818391","date":"2025-09-03T13:15:59+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-09-02T14:53:54+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-09-02T04:06:09+00:00","index":"","fulltext":""},{"type":"submitted","content":"Diagnostic Pathology","date":"2025-09-01T05:50:07+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"diagnostic-pathology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"dpat","sideBox":"Learn more about [Diagnostic Pathology](http://diagnosticpathology.biomedcentral.com)","snPcode":"13000","submissionUrl":"https://submission.nature.com/new-submission/13000/3","title":"Diagnostic Pathology","twitterHandle":"@OncoBioMed","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"em","reportingPortfolio":"BMC/SO AJ","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"d8ee0d82-1927-4f8a-8acc-df8072a0a16d","owner":[],"postedDate":"September 8th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"published-in-journal","subjectAreas":[],"tags":[],"updatedAt":"2025-10-27T16:24:34+00:00","versionOfRecord":{"articleIdentity":"rs-7257229","link":"https://doi.org/10.1186/s13000-025-01722-2","journal":{"identity":"diagnostic-pathology","isVorOnly":false,"title":"Diagnostic Pathology"},"publishedOn":"2025-10-23 16:17:22","publishedOnDateReadable":"October 23rd, 2025"},"versionCreatedAt":"2025-09-08 08:19:21","video":"","vorDoi":"10.1186/s13000-025-01722-2","vorDoiUrl":"https://doi.org/10.1186/s13000-025-01722-2","workflowStages":[]},"version":"v1","identity":"rs-7257229","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-7257229","identity":"rs-7257229","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}