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Case Report

Intracranial Inflammatory Myofibroblastic Tumor: A Literature Review and a Rare Case Misdiagnosed as Acoustic Neuroma

by
Le Zhou
1,†,
Wanqian Pan
2,†,
Renjun Huang
1,
Ziwei Lu
1,
Zhiqun You
3 and
Yonggang Li
1,4,5,*
1
Department of Radiology, The First Affiliated Hospital of Soochow University, Suzhou 215000, China
2
Department of Cardiology, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou 215006, China
3
Department of Pathology, The First Affiliated Hospital of Suzhou University, Suzhou 215000, China
4
Institute of Medical Imaging, Soochow University, Suzhou 215000, China
5
National Clinical Research Center for Hematologic Diseases, The First Affiliated Hospital of Soochow University, Suzhou 215000, China
*
Author to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Diagnostics 2023, 13(17), 2725; https://doi.org/10.3390/diagnostics13172725
Submission received: 26 July 2023 / Revised: 11 August 2023 / Accepted: 12 August 2023 / Published: 22 August 2023
(This article belongs to the Special Issue Advanced Brain Tumor Imaging)
Browse Figures
Review Reports Versions Notes

Abstract

:
Inflammatory myofibroblastic tumor (IMT) stands as a rare neoplasm, initially documented by Bahadori and Liebow in 1973; however, its biological behavior and underlying pathogenesis continue to elude comprehensive understanding. Throughout the years, this tumor has been designated by various alternative names, including pseudosarcomatoid myofibroblastoma, fibromyxoid transformation, and plasma cell granuloma among others. In 2002, the World Health Organization (WHO) officially classified it as a soft tissue tumor and designated it as IMT. While IMT primarily manifests in the lungs, the common clinical symptoms encompass anemia, low-grade fever, limb weakness, and chest pain. The mesentery, omentum, and retroperitoneum are subsequent sites of occurrence with intracranial involvement being exceedingly rare. Due to the absence of specific clinical symptoms and characteristic radiographic features, diagnosing intracranial inflammatory myofibroblastic tumor (IIMT) remains challenging. Successful instances of pharmacological treatment for IIMT indicate that surgery may not be the sole therapeutic recourse, thus underscoring the imperative of an accurate diagnosis and apt treatment selection to improve patient outcomes.

1. Introduction

IMT is a rare junctional/low-grade tumor with the potential for recurrence and progression [1]; it is mainly composed of myofibroblast spindle cells with inflammatory cell infiltration, including plasma cells, lymphocytes, and eosinophils [2]. In 2002, the WHO officially defined it as a soft tissue tumor and named it IMT [3]. The occurrence of IMT may be related to numerous factors, such as Epstein–Barr virus infection [4], surgery, trauma, etc. In addition, rearrangement and overexpression of the anaplastic lymphoma kinase (ALK) gene on chromosome 2p23 are also associated with IMT [5]. In 2000, Lawrence et al. found that the TPM3–ALK and TPM4–ALK fusion genes were related to IMT [6]. Since then, numerous ALK fusion genes have been reported, such as ATIC–ALK, CLTC–ALK, CARS–ALK, RANBP2–ALK, RRBP1–ALK, etc. [5,7,8]. In IMT, approximately 50% of ALK genes are rearranged and overexpressed; therefore, ALK positivity is helpful to diagnose IMT, but its absence does not exclude the diagnosis of IMT, particularly in adults [9,10]. The characteristic histological patterns include the fasciitis-like, compact spindle cell and hypocellular fibrous patterns [7,9]. While the most common site of occurrence is the lungs, extrapulmonary IMT tends to exhibit a more aggressive behavior and a higher susceptibility to recurrence [11]. The first reported case of IIMT was presented by SG West et al. in 1980 [12]. IIMT is extremely rare, and its clinical presentation often lacks a correlation with its histological type. Patients typically present with non-specific symptoms, such as headaches and seizures among others [13]. The preoperative diagnosis of IIMT poses challenges. Previous radiological studies have primarily depicted IIMT as a solid mass; however, Wang [14] and Park [15], among others, have also identified instances of cystic IIMT. This substantiates the notion that there is no distinct morphological component characteristic of IIMT evident in radiographic imaging.
The current body of literature concerning IIMT primarily comprises case reports, thus lacking a comprehensive overview. This article presents the first instance of hemorrhagic IIMT treated at the First Affiliated Hospital of Soochow University, which was initially misdiagnosed as an acoustic neuroma. Additionally, we conducted a comprehensive review of the relevant literature on IIMT from 1980 to 2022 using the PubMed database, aiming to enhance our understanding of this rare neoplasm.

2. Case Presentation

On 27 July 2022, a 55-year-old male presented at the Second People’s Hospital in Changshu, Jiangsu Province, China with unexplained symptoms of dizziness, unsteady walking, choking on water, and hoarseness. The attending doctor initially diagnosed an acoustic neuroma in the right cerebellopontine angle. Subsequently, the patient sought further treatment at our hospital. The patient had a history of hypertension for over 20 years but had stopped taking medication on his own for three years, perceiving stable blood pressure. Additionally, he had a history of radiotherapy for nasopharyngeal cancer 20 years ago and had been regularly followed up after discharge. Routine laboratory tests showed increased neutrophils, leukocytes, and C-reactive protein with other values within normal limits. The chest computed tomography (CT) examination revealed no abnormalities.
Cranial magnetic resonance imaging (MRI) demonstrated a circular mixed T1-weighted imaging (T1WI) and T2-weighted imaging (T2WI) signal shadow in the right cerebellopontine angle with a lesion size of approximately 3.9 × 3.2 × 3.0 cm, mixed diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) signals, and heterogeneous enhancement. The compression of the right cerebellar hemisphere and the four ventricles resulted in their displacement towards the left (Figure 1). The neuroradiologist at our hospital also diagnosed it as an acoustic neuroma. The patient underwent tumor resection, and histopathological analysis revealed a lesion comprised of fibrous collagen tissue with hemorrhagic infarcts and lamellar capillary hyperplasia. Within the lesion, there were perivascular spindle cells and epithelioid proliferation, exhibiting cellular heterogeneity and easily visible nuclear pleomorphism. Immunohistochemical staining demonstrated negativity for glial fibrillary acidic protein (GFAP), S100 protein, Oligodendrocyte transcription factor 2 (Olig-2), CD56, SOX10, and epithelial membrane antigen (EMA). Additionally, the lesion was negative for estrogen receptor (ER), progesterone receptor (PR), somatostatin receptor 2 (SSTR2), cytokeratin (CK), desmin, and CD68. The lesion displayed positivity for vimentin and exhibited scattered weak positivity for smooth muscle actin (SMA) in the vascular regions (Figure 2). Furthermore, immunostaining revealed CD34 and CD31 positivity in the vascular regions as well as erythroblast transformation specific related gene (ERG) and Ki-67 (approximately 40% in the hotspot areas) positivity (Figure 2). Based on these findings and the WHO classification guidelines (Table 1, the postoperative pathology confirmed an intracranial inflammatory myofibroblastic tumor.
Approximately one year after hospital discharge, we conducted a follow-up via phone call, during which the patient reported no notable discomfort or concerns.

3. Literature Review

This misdiagnosed case prompted us to conduct an in-depth investigation into IIMT. Due to the historical use of various names for this tumor, we conducted a comprehensive search of the PubMed database using the following keywords: “inflammatory myofibroblastic tumor,” “intracranial plasma cell granuloma,” “inflammatory pseudotumor,” “cellular inflammatory pseudotumor,” “fibrous yellow tumor,” “yellow tumor pseudotumor,” “pseudosarcomatous myofibroblast proliferation,” and “inflammatory myofibrohistiocytic proliferation”. We selected articles encompassing case reports, reviews, and other relevant studies for analysis. The literature was carefully reviewed to extract the pertinent information, such as the tumor’s location of occurrence, clinical manifestations, treatment modalities, and more. The results are shown in Table 2.
After excluding literature with unavailable content, a total of 55 cases were included in the study until October 2022. The age range of patients varied from 6 to 82 years with 23 females (41.8%) and 32 males (58.2%). While IMT primarily occurs in the lung and respiratory tract, it has also been reported in various other sites, such as the breast, esophagus, intestine, kidney, liver, lymph nodes, retroperitoneum, oral cavity, skin, stomach, thyroid, etc. However, the occurrence of IMT within the intracranial region remains exceptionally rare. From Table 2, we observed that IIMT can arise in almost all intracranial locations with the frontal (23.6%) and temporal lobes (21.8%) being the main sites. The clinical symptoms commonly included headache (56.4%) and seizures (18.2%) with headache being the predominant complaint. A few cases presented with metastasis (three cases) and recurrence (ten cases) with the earliest recurrence noted six months after treatment, and the latest recurrence occurring in the 11th year. Regarding the treatment of IIMT, various strategies were employed, including surgery, glucocorticoids, radiotherapy, chemotherapy, immunosuppressants, 6-mercaptopurine, methotrexate, non-steroidal anti-inflammatory drugs (NSAIDs), thalidomide, and amphotericin. From Table 2, we observed that most cases exhibited iso or low signal intensity on T1WI and T2WI with the DWI signal usually being low. Moreover, most of the lesions showed significant enhancement (although some were not homogeneous). Table 2 also lists the initial diagnoses made by the clinicians and neuroradiologists before the pathological results were obtained, based only on the radiological features and clinical symptoms. Interestingly, meningioma (30.9%) ranked first among the preoperative misdiagnosed diseases, similar to what has been stated in other articles; in terms of radiological presentations, IIMT resembles meningiomas [16], including enhancing features and the typical meningeal tail sign. Among all the cases listed in Table 2, there was no instance in which IIMT could be conclusively diagnosed solely based on the radiological features. This observation further underscores the intricate nature of diagnosing IIMT.

4. Discussion

IMT represents a rare neoplasm with uncertain biological behavior and underlying pathogenesis. Despite the formal definition of IMT by the WHO in 2002, certain articles published after this date still lack a clear differentiation between IMT, inflammatory pseudotumor, and other histologically akin lesions, a point also noted by Ishihara, Denis, and Vidrine [11,17,18] et al. The majority of the IIMT showed unique MRI performance: iso or low signal on TIWI and T2WI, which may be attributed to the absence of free water and mobile protons [13]. Additionally, IIMT exhibited prominent enhancement and low signal intensity on DWI. These MRI findings were different from other common intracranial parenchymal tumors, which typically present as low-intensity lesions on T1WI and high-intensity lesions on T2WI. This distinctive feature of IIMT is noteworthy in the context of radiological differentiation. In our patient diagnosed with IIMT, the T1WI and T2WI signals predominantly appeared low; however, a small area of high signal intensity was observed within the lesion. The postoperative pathology confirmed the presence of minor hemorrhage, marking the first reported case of IIMT with hemorrhage. The lesion was situated at the right cerebellopontine angle and demonstrated relatively well-defined characteristics. Consequently, the preoperative assessment by the neuroradiologist considered a right cerebellopontine angle acoustic neuroma with hemorrhage. It is noteworthy that the tumor’s atypical T1WI and T2WI signals are distinct from the usual acoustic neuroma. Considering this unique imaging characteristic, the possibility of IIMT could be contemplated, especially if there had been previous IIMT-related studies. In addition to the radiological features, the two main clinical manifestations of headache and seizures might be informative for the diagnosis of IIMT, which has been mentioned in previous reports [13,19].
In the context of this study, the panel of immune markers, including CD34, CD31, ERG, Ki-67, SMA, Vimentin, and others, assumes a pivotal role in the elucidation of both the histological attributes and the molecular profile of IIMT. CD34 and CD31 recognized endothelial markers play a crucial role in the identification of vascular constituents within the lesion [20]. The presence of positive staining for these markers indicates the presence of blood vessels and provides insight into the vascular architecture within the tumor mass. ERG, functioning as an endothelial transcription factor, further contributes to a refined comprehension of the vascular structures and the evaluation of tumor vascularity [20]. Affirmative ERG staining provides insights into the differentiation and arrangement of endothelial cells within the tumor tissue. Ki-67, a representative marker of proliferation, quantifies the proliferative activity of tumor cells. Its expression level, especially within focal hotspot regions, furnishes valuable data regarding the tumor’s growth rate and potential aggressive behavior [21]. SMA, or smooth muscle actin, denotes the presence of smooth muscle cells or myofibroblasts [22]. The scattered yet discernible weak positivity observed in the vascular regions imparts insights into the cellular composition and accentuates the presence of the smooth muscle component within the tumor. Vimentin, serving as a notable mesenchymal marker, signifies the mesenchymal origin of the tumor cells, facilitating their differentiation from other cell types [23]. The collective contribution of these immune markers contributes substantively to the comprehensive characterization of IMT, facilitating the precise diagnosis and comprehension of their biological behavior, and furnishing potential insights relevant to their management and treatment strategies.
ALK gene expression is suggestive of the development and recurrence of IIMT [17]; chemotherapeutic agents targeting ALK gene inhibition have also been used for the treatment of IIMT with good results [11]. Although some clinicians suggest that surgery is the preferred treatment option for IIMT [24], glucocorticoids have been successful in the treatment of IIMT in some cases [25,26]. Hence, a clear preoperative diagnosis of IIMT would allow for the possibility of an initial steroid-based therapeutic approach, potentially alleviating patient discomfort and reducing postoperative complications, should it prove effective.
Table 2. Information about inflammatory myofibroblastic tumor.
Table 2. Information about inflammatory myofibroblastic tumor.
Patient [Ref]LocationComplaintsMeningeal Tail SignMetastasisTreatmentRadiological ManifestationsMisdiagnosisRecurrence
17/M [12]left posterior fossaheadacheNA➖Sobviously enhancing massmeningioma➖
6/M [27]bitemporal lobedeafness, right hemiparesis, and bilateral cerebellar signs➖➖SCT: obviously enhancing massNAno recurrence at 6 years
14/F [28]right posteromedial frontal lobeheadache➖➖S+H+Robviously enhancing massmeningiomarecurrence at 6 months
48/F [29]hypothalamusdrowsiness, hyperthermia, vomiting, and headache➖➖NANANA➖
19/F [29]hypothalamusvisual loss, headaches, and drowsiness➖➖S+RNANANA
16/M [30]right frontoparietal convexityprogressive weakness in the left legNA➖SCT: iso-density massmeningioma➖
77/F [31]left frontal region and clivaldementia, urinary incontinence, and anorexia➖NAHlow SI on both T2WI and T1WI, homogeneous enhancementchronic subdural hematoma➖
40/M [32]left trigeminal nerve and left cavernous sinusdecrease in visual acuity or loss of visual field➖➖S+HT1WI: iso-SI, obviously enhancingNA➖
57/M [33]on the falx cerebri in the frontal areaheadache➖➖SNANANA
56/M [34]pituitary stalkfrontal cephalalgiasNA➖ST1WI: iso-SI, obviously enhancingNA➖
30/M [34]left cavernous sinus and tentorium cerebelliparieto-occipital cephalalgiasNA➖ST1WI: low-SINA➖
11/M [34]vermis cerebellioccipital cephalalgiasNA➖ST1WI: low-SI; T2WI: low-SI at the edge of the lesion and iso-SI in the centerNA➖
40/M [34]right cavernous sinusright fronto-orbicular cephalalgiasNA➖SCT: obviously enhancing;
TIWI, T2WI: high-SI		meningiomarecurrence at 2 years
11/M [35]left frontal lobemild headache and nausea➖➖ST1WI: slightly high-SI
T2WI: low-SI,
heterogeneous enhancement		NA➖
60/F [36]near the anterior tip of the temporal lobeheadache, grand mal seizure, and postictal confusion➕➖S+RT1WI, T2WI: low-SI, obviously enhancingNA➖
57/F [37]right cerebellopontine angleright-sided ptosis and diplopiaNA➖S+RNANANA
17/F [1]left frontalleft frontal headacheNA➖SNANArecurrence at 2 years
8/M [1]left temporalseizureNA➖SNANAno recurrence at 5 years
15/M [1]left occipitalright-sided epileptic seizureNAintracranial MTS+Robviously enhancing massNArecurrence at 6 months
18/F [38]right temporal regionheadache with occasional vomiting and blurring of vision➖➖SCT: obviously enhancing massmeningioma➖
23/M [39]right parieto-occipitalseizures➕➖S+HT1WI: low-SI
T2WI: high-SI
slightly enhancing		meningiomano recurrence at 3 years
13/M [19]right frontal lobeseizures➖➖ST2WI: hypo-intense
Obviously enhancing		NAno recurrence at 6 months
62/M [40]right fronto-parietooccipital and falxfocal motor seizures and right-sided tinnitus➕➖S+RT1WI: iso-SI
T2WI: low-SI
obviously enhancing		meningioma➖
6/M [41]right parietal regionseizure➖➖Sobviously enhancingNA➖
41/M [42]right occipital lobeepileptic seizure➖intracranial MTSobviously enhancingHigh grade glioma, brain metastasis tumorrecurrence at 11 years
22/M [43]under surface of left tentoriumheadache➕➖Sobviously enhancingmeningiomano recurrence at 19 months
64/F [44]beside the anterior parasagittal regionheadacheNA➖Sobviously enhancingmeningiomano recurrence at 3 years
70/M [45]cranial base, frontal region, floor of the third ventricleprogressive visual disturbance➖NAH+Robviously enhancingpituitary tumor, chordoma,
plasmacytoma		NA
36/F [42]left cerebellopontine angleleft-sided headache, tinnitus, and hearing lossNAMT to cervicalS+Robviously enhancingmeningiomarecurrence at 1.5 years
52/M [46]left cerebellopontine angledecreased sensation on the left side of the face, hearing loss, headache, and vomiting➖➖ST1WI: iso-SI, T2WI: low-SI
heterogeneous enhancement		trigeminal neurinoma, meningiomano recurrence at 6 months
30/F [47]left temporo-parietal extra parenchymalworsening headache and memory disturbanceNA➖SCT: iso-density mass
obviously enhancing		subacute subdural hematoma➖
48/F [47]left temporal lobeheadacheNA➖ST1: low-SI, T2: high-SI
obviously enhancing		NA➖
14/F [48]cavernous sinus, right middle cranial fossa, pterygopalatine, and infratemporalheadache➖➖H+methotrexate +6-mercaptopurineNANArecurrence at 18 months
63/M [49]right frontal lobeprogressive left hemiparesisi➖➖SMRI: the solid part of the mass was significantly enhancedNA➖
18/F [50]left frontoparietalgeneralized seizure➖➖SCT: calcifications and extensive ossification
T1: low-SI		NA➖
58/F [51]left fronto-temporalheadache➖➖S+Hobviously enhancing massNAno recurrence at 18 months
47/M [52]right cerebellum-pontine anglereduced visual acuity, hearing loss, difficulty in walking, and urinary retentionNANAH+RT1WI: iso-SI, T2WI: low-SINANA
26/F [53]left frontotemporal regionsevere headache, left eye discomfort with diplopia, left ear painNANAhigh-dose dexamethasone and thalidomideMRI: extensive enhancing, dural thickening over left frontotemporal lobesNANA
52/F [53]right lateral ventricleslipped and fell with head injuryNANASNANANA
45/M [53]right frontal regionprogressive left-sided weaknessNANASCT: right frontal dural based tumor with peritumoral edemaNANA
51/M [26]right cerebellopontine anglevertigo, diplopia, headache and fibrillationa of the tongueNA➖Hobviously enhancing massNArecurrence at 7 years
56/M [54]left basal gangliaheadaches and right-sided weakness➖➖H+biopsyTIWI: low-signal,
heterogeneous enhancement		NA➖
60/M [55]right cerebral hemispheregait disturbance and ataxia➖➖ST1WI, T2WI: iso-SI,
obviously enhancing		NA➖
82/F [56]right temporal regionheadache and memory decrease➕➖ST1WI: slightly high-SI
homogeneous enhancement		meningiomano recurrence at 13 months
38/M [57]right mastoidblurred vision and headache➖➖S+HMRI: obviously enhancing
CT: bone erosion around the tumor MRV: right sigmoid sinus occlusion		NA➖
48/F [15]right temporal regiondepression, paranoid personality, and memory impairment➖➖ST2WI: iso-SI, DWI: not limited, obviously enhancingpleomorphic xanthoastrocytoma, cystic meningioma, cystic glioma➖
20/F [58]bilateral temporal regionsheadacheNA➖ST1WI: low-SI
T2WI: mixed-SI
CT: iso-density mass
heterogeneous enhancement		NArecurrence at 7 months
10/M [2]left transverse-sigmoid junctionmastoid tenderness and headache➕➖SCT: obviously enhancingmeningioma➖
15/M [59]left parietal regionheadache, vomiting, and lethargy➖➖ST1WI: iso-SI
T2WI: low-SI
obviously enhancing		NANA
46/F [14]right temporal lobe and right cerebellar hemisphereheadache, unstable walkingNANAS+HT1WI: iso-SI
T2WI: low-SI
MRV: right transverse sinus and sigmoid sinus occlusion		malignant meningiomarecurrence at 2.5 years
21/F [5]right frontal lobebilateral blurred vision➖➖ST1WI, T2WI: low-SI
obviously enhancing		meningioma➖
54/M [14]right frontal lobeheadache➕NAST1WI: iso-SI
T2WI: low-SI
obviously enhancing		NA➖
27/M [16]right frontal parietal regionseizures➕NASobviously enhancingmeningiomaNA
80/F [60]left choroidal fissure between the amygdala and cerebral peduncleheadache, dizziness, confusion, and gait instability➖➖Sobviously enhancinganeurysm➖
NA = non-available; S = surgery; H = hormones; R = radiotherapy; NSAIDs = non-steroidal anti-inflammatory drugs; CT = computed tomography; MRI = magnetic resonance imaging; T1WI = T1-weighted imaging; T2 = T2-weighted imaging; SI = signal intensity; MRV = magnetic resonance venography; DWI = diffusion-weighted imaging. ➕ = positive; ➖ = negative.

5. Conclusions

This study presents the inaugural case of IIMT with internal hemorrhage and undertakes an all-encompassing review of pertinent literature accessible in the PubMed database. While the direct diagnosis of IIMT presents challenges, considering IIMT as a plausible differential diagnosis emerges as a feasible avenue. This approach assumes substantial significance in steering treatment strategies effectively.

Author Contributions

Y.L. designed the study. Z.L., R.H. and W.P. collected the literature. L.Z. drafted the manuscript. Z.Y. collected the pathological sections. All authors were involved in major revisions of the manuscript. All authors have read and agreed to the published version of the manuscript.

Funding

This study was supported by the program for Gusu Medical Talent of Suzhou City (grant no. GSWS2020009); the Translational Research Grant of NCRCH (grant no. 2020WSB06); and the Youth Program of Suzhou Medical Association (grant no. 2022YX-Q03).

Institutional Review Board Statement

This study was conducted in accordance with the Declaration of Helsinki and approved by the Institutional Review Board of First Hospital of Soochow University (approval code 2023-291, approved date: 7 July 2023).

Informed Consent Statement

Informed consent was obtained from all subjects involved in the study.

Data Availability Statement

All of the data in this study can be found in the PubMed database.

Conflicts of Interest

The authors declare no conflict of interest.

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Diagnostics 13 02725 g001
Figure 1. Magnetic resonance imaging (MRI) of the patient’s head with corresponding image sequences. (A) T1-weighted imaging, (B) T2-weighted imaging, (C) Diffusion-weighted imaging, (D) Apparent diffusion coefficient, (E) Fluid attenuated inversion recovery, (F) Sagittal contrast-enhanced scan, (G) Axial contrast-enhanced scan, (H) Coronal contrast-enhanced scan.
Figure 1. Magnetic resonance imaging (MRI) of the patient’s head with corresponding image sequences. (A) T1-weighted imaging, (B) T2-weighted imaging, (C) Diffusion-weighted imaging, (D) Apparent diffusion coefficient, (E) Fluid attenuated inversion recovery, (F) Sagittal contrast-enhanced scan, (G) Axial contrast-enhanced scan, (H) Coronal contrast-enhanced scan.
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Diagnostics 13 02725 g002
Figure 2. Immunohistochemical staining of the lesion demonstrated positive reactivity for vimentin (A) throughout and revealed scattered weak positivity for SMA (B) in the vascular regions. Additionally, the vascular regions exhibited positive staining for CD31 (C), ERG (D), Ki-67 (E), and CD34 (F). The original magnification is 20X.
Figure 2. Immunohistochemical staining of the lesion demonstrated positive reactivity for vimentin (A) throughout and revealed scattered weak positivity for SMA (B) in the vascular regions. Additionally, the vascular regions exhibited positive staining for CD31 (C), ERG (D), Ki-67 (E), and CD34 (F). The original magnification is 20X.
Diagnostics 13 02725 g002
Table 1. WHO classification of fibroblastic/myofibroblastic and some representative immunomarkers.
Table 1. WHO classification of fibroblastic/myofibroblastic and some representative immunomarkers.
Type of TumorRepresentative Immunomarkers
Nodular fasciitisCD34 (+), SMA (+), Desmin (−), S100 (−), ALK-1 (−), Ki-67(+)
Proliferative fasciitisSMA (+), Desmin (−), CD34 (+), S100 (−), ALK-1 (−), Ki-67 (+)
Proliferative myositisSMA (+), CD34 (+), Desmin (−), S100 (−), ALK-1 (−), Ki-67 (+)
Myositis ossificansSMA (+), Desmin (−), CD34 (−), S100(−), ALK-1 (−), Ki-67 (−)
Ischaemic fasciitisSMA (+), Desmin (−), CD34 (+), S100(−), ALK-1 (−), Ki-67 (+)
ElastofibromaSMA (+), Desmin (−), CD34 (−), S100 (−), ALK-1 (−), Ki-67 (−)
Fibrous hamartoma of infancySMA (+), Desmin (−), CD34 (+), S100(−), ALK-1 (−), Ki-67 (+)
Myofibroma/MyofibromatosisSMA (+), Desmin (−), CD34 (−), S100 (−), ALK-1 (−), Ki-67 (+)
Fibromatosis colliSMA (+), Desmin (−), CD34 (−), S100 (−), ALK-1 (−), Ki-67 (−)
Juvenile hyaline fibromatosisVimentin (+), CD34 (−), CD68 (−), SMA (−),S 100(−), Factor XIIIa (−)
Inclusion body fibromatosisVimentin (+), CD34 (−), CD68 (−), SMA (−), S100 (−), Desmin (−)
Fibroma of tendon sheathVimentin (+), CD34 (−), Desmin (−), SMA (−), S100 (−), CD68 (−)
Desmoplastic fibroblastomaVimentin (+), CD34 (−), Desmin (−), SMA (−), S100(−), CD68 (−)
Mammary-type myofibroblastomaVimentin (+), CD34 (−), Desmin (−), SMA (+), S100 (−), CD68 (−)
Calcifying aponeurotic fibromaVimentin (+), CD34 (−), Desmin (−), SMA (−), S100 (−), CD68 (−)
AngiomyofibroblastomaVimentin (+), CD34 (−), Desmin (−), SMA (+), S100 (−), CD68 (−)
Cellular angiofibromaVimentin (+), CD34 (+), Desmin (−), SMA (−), S100 (−), CD68 (−)
Nuchal-type fibromaVimentin (+), CD34 (−), Desmin (−), SMA (−), S100 (−), CD68 (−)
Gardner fibromaVimentin (+), CD34 (−), Desmin (−), SMA (−), S100 (−), CD68 (−)
Calcifying fibrous tumorVimentin (+), CD34 (−), Desmin (−), SMA (−), S100 (−), CD68 (−)
Giant cell angiofibromaVimentin (+), CD34 (−), Desmin (−), SMA (+), S100 (−), CD68 (−)
Superficial fibromatoses (palmar/plantar)SMA (+), CD34 (−), Desmin (−), S100 (−), Beta-catenin(CTNNB1) (+)
Desmoid-type fibromatosesSMA (+), CD34 (−), Desmin (−), S100 (−), Beta-catenin(CTNNB1) (+)
LipofibromatosisCD34 (+), SMA (+), Desmin (−), S100 (−), Beta-catenin(CTNNB1) (−)
Solitary fibrous tumorCD34 (+), CD99 (+), Bcl-2 (+), CD31 (−), S100 (−), Desmin (−)
Inflammatory myofibroblastic tumorALK [partly(+)], SMA (+), CD34 (+), Desmin (−), CD117 (−), S100 (−)
Low grade myofibroblastic sarcoma SMA (+), Desmin (−), CD34 (−), CD117 (−), ALK (−), S100 (−)
MyxoinflammatoryCD68 (+), CD163 (+), SMA (+), Desmin (−), CD34 (−), S100 (−)
Infantile fibrosarcomaSMA (+), Desmin (−), CD34 (−), CD99 (−), ALK (−), S100 (−)
Adult fibrosarcomaSMA (+), CD34 (−), Desmin (−), S100 (−), EMA (−), CD99 (−)
MyxofibrosarcomaCD34 (−), SMA (−), Desmin (−), S100 (−), EMA (−), CD99 (−)
Low grade fibromyxoid sarcomaCD34 (−), SMA (−), Desmin (−), S100 (−), EMA (−), MUC4 (+)
Sclerosing epithelioid fibrasarcomaCD34 (−), SMA (−), Desmin (−), S100 (−), EMA (−), INI1(SMARCB1):(+)
Ki-67: Ki-67 Antigen; Factor XIIIa: Factor XIIIa (F13A1); Beta-catenin (CTNNB1): Beta-Catenin; INI1 (SMARCB1): SWI/SNF-related matrix-associated actin dependent regulator of chromatin subfamily B member 1; Bcl-2: B-Cell Lymphoma 2.
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Zhou, L.; Pan, W.; Huang, R.; Lu, Z.; You, Z.; Li, Y. Intracranial Inflammatory Myofibroblastic Tumor: A Literature Review and a Rare Case Misdiagnosed as Acoustic Neuroma. Diagnostics 2023, 13, 2725. https://doi.org/10.3390/diagnostics13172725

AMA Style

Zhou L, Pan W, Huang R, Lu Z, You Z, Li Y. Intracranial Inflammatory Myofibroblastic Tumor: A Literature Review and a Rare Case Misdiagnosed as Acoustic Neuroma. Diagnostics. 2023; 13(17):2725. https://doi.org/10.3390/diagnostics13172725

Chicago/Turabian Style

Zhou, Le, Wanqian Pan, Renjun Huang, Ziwei Lu, Zhiqun You, and Yonggang Li. 2023. "Intracranial Inflammatory Myofibroblastic Tumor: A Literature Review and a Rare Case Misdiagnosed as Acoustic Neuroma" Diagnostics 13, no. 17: 2725. https://doi.org/10.3390/diagnostics13172725

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