Nodular Fasciitis: A Case Series Unveiling Novel and Rare Gene Fusions, Including Two Cases with Aggressive Clinical Behavior

Abstract

Nodular fasciitis is a benign myofibroblastic tumor characterized by rapid growth and spontaneous regression. While nodular fasciitis is typically an indolent process, rare cases with benign morphologic features have developed metastases. Conversely, nodular fasciitis with malignant histologic features and benign clinical course have also been reported. In this study, we present seven nodular fasciitis cases with novel USP6 gene fusion partners, in addition to two cases with rare fusions that displayed aggressive clinical behavior. The cohort comprised five females and four males with a median age of 36 years (range 13–59). Tumors were located in the forearm (n=3), thigh (n=2), and shoulder, abdominal wall, chest wall, and oral cavity (one each), ranging from 1.4 to 24.0 cm in size (median, 2.2 cm). Except for the clinically aggressive cases, patients presented with painless masses of varying onset from days to months. Of the clinically aggressive cases, one patient presented with a slowly growing subfascial thigh/hip mass over nine years, leading to erosion of the femur and pelvis; the other presented with a painful subfascial thigh mass of several months’ duration. Histologically, all cases, including the clinically aggressive ones, showed conventional nodular fasciitis features without nuclear pleomorphism or atypical mitotic figures; one case with aggressive clinical behavior exhibited focal infarction type necrosis. Break-apart FISH analysis using USP6 flanking probes failed to detect USP6 rearrangement in two cases (false negatives) and was inconclusive in one case. Next-generation RNA sequencing identified USP6 fusions in all cases. The clinically aggressive cases showed fusions with COL1A1 (exon 1) and PPP6R3 (exon 1), while novel fusions were identified in the remaining cases including EIF4A1 (exon 1), FILIP1L (exon 2), NF1 (exon 33), OMD (exon 1), PFN1 (exon 1), RLIM (exon 1), and SETD5 (exon 1). Six patients underwent surgical resection; three were managed conservatively, with two experiencing spontaneous tumor resolution. Of the clinically aggressive cases, one patient had progression of the tumor with erosion of the underlying bone, and the second patient developed local recurrence at 14 months and lung metastasis at 19 months, ultimately dying of disease at 22 months. The remaining patients showed no recurrence or metastasis. Our findings expand the spectrum of USP6 gene fusion partners in nodular fasciitis and, for the first time, report cases with conventional morphology exhibiting aggressive behavior, including death. These observations raise the question of whether a subset of deep lesions with conventional nodular fasciitis histology but unusual clinical features, such as large tumor size, represents malignant nodular fasciitis or alternatively a nodular fasciitis-like myofibroblastic sarcoma.

INTRODUCTION

Nodular fasciitis is a common soft tissue tumor, generally occurring in children and young adults, with predilection of the head and neck, trunk, and upper extremity regions^1–3. It was initially described as a pseudo-sarcomatous, self-limiting process, known for its rapid growth and painful nature, often followed by complete regression³. Historically, the diagnosis of nodular fasciitis was primarily based on its characteristic histologic and clinical features. However, recent advances in molecular diagnostics have unveiled recurrent gene fusions, notably involving the USP6 (Ubiquitin-specific protease 6) gene, supporting a neoplastic rather than a purely reactive etiology^4,5. Given the self-limited nature of the lesion, nodular fasciitis could serve as a model of the so-called “transient neoplasia” concept⁴. Rearrangements involving the same gene have also been demonstrated in aneurysmal bone cysts, myositis ossificans, fibro-osseous pseudotumor of the digits, and a subset of cellular fibromas of the tendon sheath^6–9. MYH9 is the most common rearranged gene partner in nodular fasciitis, accounting for approximately 75% of USP6 alterations in this group⁵. To date, more than 25 gene partners have been reported including CALU, COL6A2, COL3A1, COL1A2, EIF5A, EMP1, NR1D1, SPARC, SERPINH1, NR1D1, THBS1, THBS2 and PPP6R3 amongst others ^5,10–15. These translocations operate through a “promoter swapping” mechanism, where the translocation places the entire coding region of USP6 next to the promoter of the partner gene, leading to elevated USP6 gene expression⁵.

Although the majority of nodular fasciitis cases are histologically bland and typically follow a benign clinical course, rare instances have been reported where morphologically benign nodular fasciitis demonstrates aggressive clinical behavior, including metastasis. Guo et al. described a subcutaneous mass in a 42-year-old female with conventional nodular fasciitis histology and a PPP6R3::USP6 gene fusion, which exhibited multiple recurrences involving deep soft tissues and distant metastases over a prolonged 15-year period¹⁰. Another deep soft tissue mass with the same gene fusion, presenting in a 27-year-old male, also displayed benign histology but grew to 12.9 cm over two years, further highlighting the potential for aggressive behavior in nodular fasciitis despite a benign appearance¹⁶. Conversely, morphologically malignant nodular fasciitis cases with benign clinical course have been documented. Tomassen et al. reported a case of malignant-appearing nodular fasciitis with a COL6A2::USP6 gene fusion in a 10-year-old male, who remained disease-free 22 months after follow-up¹¹. Another morphologically malignant nodular fasciitis harboring CALD1::USP6 gene fusion was reported; however, follow-up data was not available. In this study, we present a series of nodular fasciitis cases with novel USP6 gene fusion partners. Additionally, we report two cases harboring rare fusion partners (COL1A1 and PPP6R3) which exhibited aggressive clinical behavior.

MATERIAL AND METHODS

Case selection and study cohort

The archival files of the Pathology Department of Memorial Sloan Kettering Cancer Center, Stanford University Hospital and Bioptical Laboratory, Ltd, Plzeň, Czech Republic along with the consultation files of the authors (AA, GWC, KL) were searched for unpublished cases of nodular fasciitis harboring novel gene fusions. The electronic medical records were searched for clinical data including age, sex, anatomic site, tumor size, and treatment. In addition, follow up data, when available, including local recurrence, distant metastasis, and follow-up period were gathered. All slides were reviewed, and pathologic findings were recorded encompassing cytomorphology, architectural growth, mitotic index (per 2 mm²), presence of atypical mitotic figures, and tumor necrosis. All available immunohistochemical stains were reviewed and their expression were recorded. The study was approved by an umbrella Institutional Review Board protocol of the participating institutions.

Fluorescence in situ hybridization

In three cases, fluorescence in situ hybridization (FISH) on interphase nuclei derived from formalin-fixed paraffin embedded (FFPE) 4 μm sections was conducted using custom designed probes of bacterial artificial chromosomes (BAC) flanking USP6 gene. BAC clones were selected based on the UCSC genome browser (http://genome.ucsc.edu) as previously published¹⁷. The BAC clones were obtained from BACPAC sources of Children’s Hospital of Oakland Research Institute (CHORI) (Oakland, CA) (https://bacpacresources.org). FISH was conducted using a dual-color break-apart probe for USP6 (Zytovision, 17p13.2), with a cut-off of 10% for normal variation in FFPE tissue sections. One hundred consecutive nuclei were examined for the presence of USP6 rearrangement using a Zeiss fluorescence microscope (Zeiss Axioplan, Oberkochen, Germany) under the control of Isis 5 software (Metasystems, Waltham, MA). At least 10% of the nuclei with a break-apart signal was needed to interpret a FISH test as positive for rearrangement. Nuclei displaying an incomplete set of signals were excluded from the scoring.

Targeted RNA sequencing

In two cases, targeted RNA sequencing, was performed using Archer FusionPlex (Archer, Boulder, CO), an anchored multiplex PCR-based assay, targeting specific exons in 129 genes¹⁸. In the remaining cases, the TruSight RNA Fusion Panel (Illumina, San Diego, CA) was performed, as previously described¹⁹. Briefly, RNA was extracted from FFPE tissue using Amsbio’s ExpressArt FFPE Clear RNA Ready Kit (Amsbio, Cambridge, MA). Fragment length was evaluated with an RNA 6000 chip on an Agilent Bioanalyzer (Agilent Technologies, Santa Clara, CA). RNA-sequencing libraries were prepared using 20 to 100 ng total RNA. The samples were subjected to targeted RNA sequencing on an Illumina MiSeq (~3 million reads per sample). All reads were independently aligned with STAR (version 2.3) and BowTie2 against the human reference genome (hg19) for Manta-Fusion and TopHat-Fusion analysis, respectively.

RESULTS

Cohort summary

The tumors occurred in five females and four males, with a median age of 36 years (range 13–59 years). The tumors involved forearm (n=3), thigh (n=2), shoulder (n=1), abdominal wall (n=1), chest wall (n=1) and oral cavity (n=1). The tumors were primarily located in the subcutis (n=5), with the remaining found in the muscle (n=2), the subcapsular region of the shoulder (n=1), and the oral submucosa (n=1). They ranged from 1.4 to 24.0 cm, with a median size of 2.2 cm. Five patients (cases 1, 2, 3, 4, and 7) presented with a painless mass, with the onset varying from a few days to several months. Case 8 exhibited a slowly growing mass in the thigh/hip region over a period of nine years, which subsequently led to erosion of the femur and pelvis. Case 9 presented with a painful mass of several months’ duration. Both cases 8 and 9 were subfascial. Clinicopathologic characteristics of the cases are summarized in Table 1.

Table 1:

Clinicopathologic and follow-up data of the cohort cases

Case #	Age (y)/ Sex	Site	Size (cm)	Mitotic index (/10 HPF)	Atypical mitotic figures	IHC	LR/M	Treatment	Status at last FU	FU period (mo)	USP6 FISH	RNA Seq
1	51M	Abdominal wall	2.2	1/10	No	B-catenin (−)	No	Observation	NED	9	Inconclusive	FILIP1L(exon 2) ::USP6(exon 1)
2	43F	Chest wall	1.4	3/10	No	SMA (+), B-catenin (−), S100 (−), CD34 (−)	No	Resection	NED	10	Negative	PFN1 (exon 1):: USP6 (exon 3)
3	34F	Forearm	2.0	NA	No	Not done	NA	Resection with + margin	NA	NA	Negative	RLIM (exon 1):: USP6 (exon 2)
4	22F	Forearm	1.5	1/10	No	SMA (+), desmin (−), caldesmon (−), CD31 (−), CD34 (−)	No	Resection	NED	10	Not done	SETD5 (exon 1) ::USP6 (exon 1)
5	36M	Shoulder	NA	NA	No	Not done	NA	Resection	NA	NA	Not done	NF1(exon 33)::USP6 (exon 8)
6	13F	Oral cavity	NA	NA	No	Not done	NA	Resection	NA	NA	Not done	OMD (exon 1)::USP6(exon 2)
7	42M	Forearm	3.0	2/10	No	SMA(+/−), S100 (−), CD34 (−), desmin (−)	No	Observation	NED	NA	Not done	EIF4A1(exon 1) ::USP6 (exon 7)
8	59F	Thigh/Hip	24	<1/10	No	SMA (+), desmin (+/−), S100(−), CD34 (−), MUC4 (−), B-catenin (−)	NA	Observation	AWD	108	Not done	PPP6R3 (exon 1) ::USP6 (exon 1)
9	36M	Thigh	13.6	15/10	No	SMA (+), MSA (+/−), desmin (−), caldesmon (−), MUC4(−)	LR (14), M (lungs, 19)	Resection with + margin	DOD	22	Not done	COL1A1 (exon 1) ::USP6 (exon 1)

M, male; F, female; NA, not available; SMA, smooth muscle actin; MSA, muscle specific actin; NED, no evidence of disease; AWD, alive with disease; DOD, died of disease; FU, follow-up; mo, months; FISH, fluorescence in situ hybridization; Seq; sequencing.

Histopathologic findings

The tumors were composed of plump spindle cells with ovoid nuclei, fine chromatin and small nucleoli. No nuclear hyperchromasia or pleomorphism was observed in any of the cases. The tumors exhibited variable cellularity ranging from low to intermediate with a storiform fibrotic to myxoid stroma, and displayed a torn, feathery, or tissue culture-like appearance. Dispersed collagen was noted in all cases, with keloid-type collagen present focally in five cases (Fig. 1A–1B, Fig. 2A–2B). Extravasated erythrocytes were identified in all cases (Fig. 1C), and osteoclast-like giant cells were observed in four. The lesion borders showed at least focal extension into the adjacent subcutis or skeletal muscles. Mitotic activity was predominantly low, but one case (case 9) demonstrated an increased mitotic count, reaching up to 15 mitoses per 2 mm² (Fig. 1D). No atypical mitotic figures were identified in any of the cases. Infarction type tumor necrosis was observed in one case (case 9).

Fig 1A-1D: Histopathologic features of nodular fasciitis.

A-B, Case 1 (FILIP1L::USP6), Nodular fasciitis exhibiting alternating cellularity with focal myxoid stroma and a “tissue culture-like” appearance. Keloid-type collagen was identified in a subset of cases (A, 100x, B, 200x). C-D, Case 2 (PFN1::USP6), Cellular nodular fasciitis exhibiting a storiform proliferation of bland spindle cells with ovoid nuclei, fine chromatin, and small nucleoli, along with numerous extravasated erythrocytes. Mitotic figures ranged from <1/10 high-power fields up to 15/10 high-power fields; however, no atypical figures were identified in any case from this series (C, 100x, D, 200x)

Fig 2A-2D: Histopathologic features of nodular fasciitis with aggressive clinical behavior.

A-B, Case 9 (COL1A1::USP6), Nodular fasciitis exhibiting a storiform proliferation of bland spindle cells in a fibrotic stroma with extravasated erythrocytes and scattered mitotic figures; focal infarction type necrosis was noted (A-B, 200x). C-D, Case 8 (PPP6R3::USP6) Nodular fasciitis exhibiting a bland spindle cell proliferation arranged in a storiform pattern and embedded in a fibrotic stroma. Atypical histologic features were not seen in either case (C, 100x, D, 200x).

Immunohistochemistry revealed non-specific staining patterns; however, smooth muscle actin (SMA) was expressed in all tested cases in a “tram-track” pattern (5/5). Desmin showed focal expression in 1/4 cases. Both S100 and CD34 were consistently negative across all samples. β-catenin immunostaining did not demonstrate aberrant nuclear expression in any of the tested cases (0/3).

Fluorescence in situ hybridization

Break-apart FISH analysis using 3’ and 5’ USP6 locus flanking probes did not demonstrate USP6 rearrangement in two cases, representing false negatives. In one tested case, USP6 gene rearrangement was detected in 10% of nuclei, showing a small separation gap, rendering the results inconclusive.

Targeted RNA sequencing

NGS RNA sequencing detected USP6 fusion in all cases. The USP6 breakpoints included exon 1 (n=4), exon 2 (n=2), exon 3 (n=1), exon 7 (n=1) and exon 8 (n=1). USP6 fusions encompassed the following novel partners: EIF4A1 (exon 1), FILIP1L (exon 2), NF1 (exon 33), OMD (exon 1), PFN1 (exon 1), RLIM (exon 1) and SETD5 (exon 1). Case 8 and 9 harbored PPP6R3 (exon 1) and COL1A1 (exon 1) partners respectively. Schematic visualization of the novel fusions and predicted retained protein domains using Arriba software (https://github.com/suhrig/arriba) are represented in Fig. 3A–3E and Supplementary Fig. 1.

Fig. 3A-3E: Schematic visualization of detected novel fusion transcripts and predicted retained protein domains in nodular fasciitis.

A, FILIP1L (exon 2)::USP6 (exon 1); B, PFN1 (exon 1)::USP6 (exon 3); C, RLIM (exon 1)::USP6 (exon 2); D, SETD5 (exon 1)::USP6 (exon 1); E, EIF4A1 (exon 1)::USP6 (exon 7).

Clinical follow-up

Six patients underwent surgical resection, while three were managed with observation; in two of these patients, the tumors spontaneously resolved. However, in case 8, the mass was unresectable, necessitating observation. Over time, the tumor progressively eroded the underlying femur and pelvis. Clinical follow-up was available for six cases. Case 9 experienced both local recurrence and metastasis, with recurrence at 14 months and metastasis to the lung at 19 months. No other cases showed disease recurrence or metastasis. One patient (case 9) died of the disease at 22 months, one patient was alive with disease, and four patients remained disease-free at 9 to 10 months of follow-up.

DISCUSSION

The USP6 gene encodes ubiquitin carboxyl-terminal hydrolase 6, a key component of the ubiquitin-proteasome system. This enzyme exhibits pleiotropic effects, participating in various cellular processes including intracellular trafficking, protein catabolism, inflammatory signaling cascades, cell transformation, and osteoblast differentiation⁶. Rearrangement of the USP6 gene is a diagnostic hallmark of nodular fasciitis, with studies showing its presence in up to 92% of cases⁴. MYH9, a member of the non-muscle myosin class II family, is the most commonly rearranged gene in nodular fasciitis, with over 25 additional gene partners reported to date. In this study, we present seven cases of nodular fasciitis featuring novel USP6 gene fusions. Additionally, we report two cases with rare gene fusions that, despite exhibiting conventional histology, displayed aggressive clinical behavior with one case resulting in the patient’s death.

A review of the literature identified, to the best of our knowledge, eight reported cases of histologically atypical or histologically malignant nodular fasciitis^{11,13,14,16,20,21}. The cases occurred in 6 males and 2 females, aged between 1.8 and 58 years. The tumors occurred in various anatomical sites, primarily in the extremities such as the thigh, upper arm, forearm, and wrist. The tumors ranged from 2.2 to 6.3 cm when specified. Histologically, nuclear pleomorphism was observed in three cases, while tumor necrosis was present in one case. Most tumors exhibited increased mitotic activity, and atypical mitotic figures were present in seven cases. Notably, one case with USP6::PPP6R3 gene fusion showed gene fusion product amplification, which might be responsible for the atypical/malignant histology. Other reported fusion partners included COL6A2, CALD1, EIF5A, PAFAH1B1, RRBP1, and THBS2. Surgical resection was the primary treatment modality for all patients. At the last follow-up, which ranged from 12 to 144 months, all patients had no evidence of disease, highlighting a generally favorable prognosis even among patients with atypical or malignant histology. Although none of our cases displayed overtly atypical or malignant histological features, two cases involving PPP6R3 and COL1A1 gene fusions exhibited aggressive clinical behavior. The correlation between histological features or gene fusion partners and clinical outcomes remains unclear, and more cases are needed for a better understanding. Of note, assessment for fusion product amplification was not feasible in our cases as FISH was not performed. Furthermore, DNA sequencing which might have uncovered genetic alterations potentially contributing to the aggressive clinical behavior observed in our cases, was also not performed. However, this possibility appears less likely, as targeted DNA sequencing in three out of eight atypical or histologically malignant nodular fasciitis reported did not identify such alterations^{10,11,13,14,16,20,21}. Notably, these subfascial cases were characterized by exceptionally large tumor sizes, measuring 24.0 cm and 13.6 cm, respectively. This unusual presentation may serve as a critical red flag for potential clinical aggressiveness, highlighting the importance of closer evaluation and monitoring in such cases. Table 2 provides a summary of the reported cases of histologically atypical and histologically malignant nodular fasciitis.

Table 2:

Literature review of reported histologically atypical and malignant nodular fasciitis cases

Study	Age (y)	Sex	Site	Size (cm)	Nuclear pleomorphism/Necrosis	MI (/HPFs)	Atypical mitotic figures	Gene fusion	Treatment	LR/DM	Status at last FU	FU period (mo)
Qiu et al.	1.8	M	Left scapular area	2.6	No/No	10/10	Yes	PAFAH1B1 (exon 1)::USP6 (exon 9)	Resection	No	NED	39
Tomassen et al.	10	M	Chest wall	2.4	Yes/No	Numerous	Yes	COL6A2 (exon 1)::USP6(exon 9)	Resection	No	NED	22
Lenz et al.	41	F	Forearm	2–3	No/No	5/5	Yes	EIF5A (exon 1)::USP6 (exon 1)	Resection	NA	NA	NA
Papke at al.	7	M	Dorsal wrist	2.2	Yes/No	7/10	Yes	CALD1 (exon 3)::USP6 (exon 2)	Resection	NA	NA	NA
Teramura et al.	27	M	Upper arm	6.3	Yes/Yes	5/10	NA	PPP6R3 (exon 1)::USP6 (exon 1)	Resection	No	NED	12
Arcovito et al.	56	M	Shoulder	NA	No/No	Increased	Yes	THBS2::USP6	Resection	No	NED	34
Arcovito et al.	29	F	Thigh	NA	No/No	Increased	Yes	RRBP1::USP6	Resection	No	NED	42
Arcovito et al.	58	M	Thigh	NA	No/No	Increased	Yes	Unknown partner (USP6 rearranged)	Resection	No	NED	38

M, male; F, female; y, year; mo, months; FU, follow-up; NED, no evidence of disease; AWD, alive with disease; LR, local recurrence; DM, distant metastasis; HPF, high-power fields

All but one of the novel gene fusions discovered in our cohort exhibit a mechanism similar to that of other known USP6 fusions in nodular fasciitis and related neoplasms, where the promoter of the fusion partner gene drives transcription of the USP6 coding region⁵. The exception is the NF1::USP6 gene fusion, which retains not only the promoter but also the GTPase-activator protein domain within the fusion. The significance of this gene fusion remains uncertain. Filamin A interacting protein 1-like (FILIP1L) is a tumor suppressor gene, identified in several types of cancer, including colorectal cancer²². PFN1 is the gene that encodes profilin 1, a protein that binds to G-actin and plays a crucial role in cytoskeletal dynamics and actin filament polymerization. Mutations in PFN1 have been linked to amyotrophic lateral sclerosis²³. RLIM (also known as RNF12) encodes an E3 ubiquitin ligase that plays a role in X-chromosome inactivation and other cellular processes²⁴. SETD5, encodes a histone methyltransferase involved in regulating gene expression, embryonic development, and brain function, with mutations in this gene associated with intellectual disability and autism spectrum disorders^25,26. Rearrangements involving FILIP1L, PFN1, RLIM and SETD5 genes have not been reported in tumors to our knowledge.

OMD (Osteomodulin) belongs to a family of leucine-rich repeat proteoglycans located on chromosome 9q22, which also includes asporin, extracellular matrix protein 2 (ECM2), and osteoglycin²⁷. OMD::USP6 gene fusion, reported in our cohort, has been reported in one case of aneurysmal bone cyst²⁸. The NF1 gene encodes neurofibromin, a cytoplasmic, multidomain protein that negatively regulates the RAS cellular proliferation pathway and is involved in other functions such as adenylate cyclase activation, cell adhesion, motility, and suppression of epithelial-mesenchymal transition; its inactivation as a classical tumor suppressor gene is responsible for neurofibromatosis type 1^29,30. Although rare, NF1 rearrangements in soft tissue tumors have been reported. Notably, a SETD2::NF1 gene fusion was identified in a case of pediatric spindle cell neoplasm, not otherwise specified, which demonstrated a benign clinical course ³¹. EIF4A1 is an ATP-driven RNA helicase that plays a key role in initiating cap-dependent translation by unwinding secondary structures within the 5’-untranslated region (5’-UTR) of mRNAs³². This unwinding facilitates ribosome binding and scanning, functioning as part of the eIF4F complex³². Although rearrangements of the EIF4A1 gene have not been reported to date, a fusion involving EIF5A, a gene that is somewhat functionally related to EIF4A1, and the USP6 gene has been identified in nodular fasciitis²⁰.

Interestingly, in our cohort, break-apart FISH for USP6 was negative in two cases and inconclusive in one. Several studies have highlighted the high sensitivity and specificity of USP6 FISH in diagnosing nodular fasciitis. Erickson-Johnson et al. reported a sensitivity of 93% and a specificity of 100% for USP6 FISH⁴. Additionally, Shin et al. reported a sensitivity of 86% and a specificity of 100%³³. The discrepancy between negative USP6 FISH results and positive RNA sequencing findings is not clear and could be the result of technical limitations, suboptimal tissue quality or the result of cryptic rearrangements. In case 2, both fusion partners (PFN1 (17p13.2) and USP6 (17p13.2)) are in proximity, leading to an intrachromosomal rearrangement that may not be detectable by FISH due to its limited spatial resolution. Thus, a negative FISH result does not exclude the diagnosis of nodular fasciitis, and confirmation with RNA sequencing can be pursued if molecular confirmation is deemed necessary.

In conclusion, we expand the spectrum of fusion partners involved in the characteristic USP6 gene fusion in nodular fasciitis. Additionally, we report two cases with otherwise conventional histology that exhibited aggressive clinical behavior, one of which represents the first documented instance of death associated with nodular fasciitis. These observations raise the question of whether a subset of deep lesions with conventional nodular fasciitis histology but unusual clinical features, such as large tumor size, represents malignant nodular fasciitis or alternatively a nodular fasciitis-like myofibroblastic sarcoma.

Supplementary Material

Supplementary Figure 1

Supplementary Fig. 1: Schematic visualization of NF1::USP6 and OMD::USP6 fusion transcripts and predicted protein domain in nodular fasciitis. A, NF1 (exon 33)::USP6 (exon 8); B, OMD (exon 1)::USP6 (exon 8).

DATA AVAILABILITY

The data generated or analyzed during this study are included in this article. Further inquiries can be sent to the corresponding author.