Postoperative Spindle Cell Nodule Research Articles

Bladder Postoperative Spindle Cell Nodule: Malignant Mimicry in the Postoperative Setting

Bladder Postoperative Spindle Cell Nodule: Malignant Mimicry in the Postoperative Setting

USP6-associated neoplasm as a tentative subset of postoperative spindle cell nodule.

Postoperative spindle cell nodule (PSCN) is a pseudosarcomatous proliferative lesion of unclear molecular genetic origins. We examined seven patients with PSCN, using routine haematoxylin-eosin (H&E) slide preparations and a series of immunostains. The latter targeted keratin, vimentin, α-smooth muscle actin (SMA), anaplastic lymphoma kinase (ALK [D5F3]), and other proteins. Ubiquitin-specific peptidase 6 (USP6) and anaplastic lymphoma kinase (ALK) gene rearrangements were also analysed by fluorescence insitu hybridization (FISH). There were histories of prior surgical intervention (n=6) or trauma (n=1) in all seven patients. All lesions were highly cellular and mitotically active spindle cell proliferations, with no cytologic atypia, nuclear pleomorphism, or aberrant mitoses. Immunohistochemical (IHC) staining disclosed focal, weak keratin positivity in two lesions, whereas vimentin (diffuse, strongly positive) and SMA (tram-track pattern) were present in each instance, and ALK (D5F3) was entirely negative. FISH analysis confirmed USP6 gene rearrangements in all seven cases, showing no ALK gene rearrangements. RNA sequencing results showed an MYH9::USP6 gene fusion in only one lesion (No. 6). A subset of PSCN is marked by USP6 gene rearrangements, a genetic feature of nodular fasciitis (NF). Given its similarity to NF, a designation as USP6-associated neoplasm (UAN) seems reasonable, signifying a transient clonal neoplastic lesion.

Inflammatory Myofibroblastic Tumour in Antimesenteric Border of Descending Colon of Children: A Case Report

Inflammatory myofibroblastic tumour (IMT) occurring at intraabdominal sites in children has rarely been described. Inflammatory pseudotumour is a soft tissue lesion that may be confused with a sarcoma. It is abbreviated as IMT. Inflammatory myofibroblastic tumour, also known as soft tissue tumours, atypical fibromyxoid tumours, pseudosarcomatous fibromyxoid tumour, plasma cell granuloma, pseudosarcomatous myofibrotic proliferation, post-operative spindle cell nodules. In this paper, we describe a case of inflammatory myofibroblastic tumour (IMT) with an unusual constellation of clinical, pathological findings. A 10-year-old girl had an 7-cm intraabdominal mass accompanied by severe anemia, fever, constipation, weight loss, thrombocytosis, elevated erythrocyte sedimentation rate. Laparotomy was performed. The final pathologic diagnosis was IMT. At the most recent follow up (12months) after excision of the tumour, the patient was symptom-free and there was no evidence of tumour recurrence.J. Paediatr. Surg. Bangladesh 3(1): 47-50, 2012 (January)

Inflammatory Myofibroblastic Tumor of the Bladder

We illustrate a case of an inflammatory myofibroblastic tumor (IMT) involving the bladder in a woman with dysuria and review the literature and differential diagnosis. Inflammatory myofibroblastic tumor, also referred to as pseudosarcomatous myofibroblastic proliferation, is a rare lesion that can arise in the genitourinary system and is characterized by a fascicular arrangement of myofibroblasts with admixed inflammatory cells and slitlike vessels. Urinary bladder IMT can be a diagnostic pitfall because its histologic features (brisk mitoses, invasion into muscularis propria, and prominent nucleoli) can mimic malignancy. The differential diagnosis of urinary bladder IMT includes sarcomatoid carcinoma and leiomyosarcoma. Diagnostic features such as bland nuclear chromatin, ganglion-like cells, pale eosinophilic cytoplasm with long processes, overexpression of anaplastic lymphoma kinase (immunohistochemistry or gene rearrangement studies), and the absence of atypical mitoses help distinguish IMT from its malignant mimics. Current controversies regarding postoperative spindle cell nodule and IMT are discussed.

Postoperative spindle cell nodule of the bladder: A case report and review of the literature.

Postoperative spindle cell nodule (PSCN) of the bladder is a rare condition. It is a type of benign lesion frequently misdiagnosed as sarcomatoid carcinoma on the basis of similar cell morphology. The present report describes a tumor affecting a 71-year-old male who had undergone three transurethral resections. Pathological results suggested a diagnosis of sarcomatoid carcinoma, and therefore a radical cystectomy was performed. However, the tumor was later identified as a PSCN. In order to prevent such misdiagnosis, this study reviews relevant articles concerning postoperative spindle cell nodules of the bladder and compares PSCN and sarcomatoid carcinomas to identify specific characteristics of PSCN. Finally, the report emphasizes the importance of careful pathological examination in rare cases such as PSCN and sarcomatoid carcinoma.

Pseudosarcomatous Fibromyxoid Tumor of the Bladder and Prostate: A Case Report

Pseudosarcomatous fibromyxoid tumor (PSFT) is a rare pseudotumor of the genitourinary (GU) system that typically presents with gross hematuria. These tumors are benign, locally aggressive tumors. Metastasis has never been reported. Pathology is significant for spindle cell proliferation without malignant nuclear features that are commonly seen in sarcomas. Herein, we report a case of an 8-centimeter PSFT found within the bladder of a 71-year-old gentleman with gross hematuria. We also review the literature on genitourinary pseudotumors, including postoperative spindle cell nodules (PSCN). Lastly we describe the importance of considering these types of tumors in the presence of a GU mass as early identification may preclude the patient from receiving unnecessary imaging and aggressive treatment measures.

Low-Grade Myofibroblastic Proliferations of the Urinary Bladder

Myofibroblastic proliferations of the urinary bladder, which share some similarities with nodular fasciitis, were first reported in 1980. Since then, they have had several designations, the most frequently used being inflammatory myofibroblastic tumor. Based on both histopathologic and prognostic grounds, some authors prefer the term pseudosarcomatous myofibroblastic proliferation, at least for some of the proliferations. These same scientists also assimilate the so-called postoperative spindle cell nodules with the pseudosarcomatous myofibroblastic proliferations. Little is known about these low-grade myofibroblastic proliferations. To review the literature about low-grade myofibroblastic proliferations occurring in the urinary bladder. Textbooks and literature review. We obtained most of the clinicopathologic peculiarities from a patient population composed of the most-relevant, previously reported cases. The low-grade myofibroblastic proliferations of the urinary bladder are rare lesions affecting males more often than they do females. The most-common signs and symptoms are hematuria and dysuria. Histopathologically, they are spindle cell proliferations in a loose myxoid stroma, even though compact proliferations or hypocellular fibrous patterns can be found. Immunohistochemistry is quite nonspecific, except for ALK-1 positivity (20%-89%). Fluorescence in situ hybridization has demonstrated clonal genetic aberrations involving the ALK gene in 50% to 60% of cases. After surgery, only 6% of patients experience local recurrence, without metastases or deaths from the disease. Malignant transformation has been reported exceptionally. These myofibroblastic proliferations are probably part of a continuum with, at one end, benign pseudosarcomatous proliferations and, at the opposite end, more-aggressive lesions. Because of the frequently indolent clinical course, aggressive treatment would be unjustified.

Fine Needle Aspiration Cytology of Postoperative Spindle Cell Nodule in Neck after Thyroidectomy: A Case Report

Although postoperative spindle cell nodules have occasionally been found in the lower genitourinary tract,1-3 their presence in post thyroidectomy sites has been reported in only one case.4 In addition, diagnosis by fine needle aspiration (FNA) has not been established. Here, we report on characteristic cytologic findings for a postoperative spindle cell nodule arising in the post-thyroidectomy site.

Postoperative spindle cell nodule after thyroidectomy: A case mimicking recurrence with anaplastic transformation of thyroid cancer

Here, we report a case of a postoperative spindle cell nodule that mimicked recurrence with anaplastic transformation after thyroidectomy. The course of the disease is described. The mass was studied morphologically and immunohistochemically. A 31-year-old woman underwent total thyroidectomy for papillary thyroid carcinoma. A mass suspected of recurrence was found 14 months later and caused dysphagia and dyspnea. An (18)F-fluorodeoxyglucose positron emission tomographic ((18)F-FDG-PET) scan showed a lesion with high uptake; however, a fine-needle aspiration biopsy (FNAB) was inconsistent with recurrent cancer. The mass was resected and was composed of elongated spindle cells, with eosinophilic cytoplasm within a myxoid background. Immunohistochemical staining was strongly positive for vimentin, focally positive for smooth muscle actin, desmin, and p53, and negative for cytokeratin AE1/AE3, Cam5.2, epithelial membrane antigen (EMA), and anaplastic lymphoma kinase (ALK-1). Although postoperative spindle cell nodules are rare after thyroid surgery, it should be considered in the differential diagnosis for recurrent masses at the operative site.

Bladder Cancer Therapy Related Histopathologic Changes

Various forms of modern therapy of urinary bladder cancer are associated with characteristic changes. Surgical therapy related morphology alterations usually do not present significant differential diagnostic problems. Postoperative spindle cell nodule may resemble a spindle cell sarcoma, but the fact that it arises within 120 days following surgery makes the diagnostic interpretation less cumbersome. Changes induced by BCG include epithelial denudation of the bladder, small superficial granulomas and chronic inflammation. Other forms of immunotherapy are associated with formation of lymphatic follicles or diffuse lymphocytic infiltrates. Radiation induced changes may appear many years after therapy and include atypia, bizarre appearance and multinucleation of urothelial cells. In the late phase, stroma is particularly affected. It is important not to misdiagnose radiation induced changes for CIS or invasive nested carcinoma. Chemotherapy-induced atypia may be recognized cytologically and histologically by the characteristic changes of the nuclear/cytoplasmic ratio, multiple nuclei, nuclear vacuolization, and architectural disturbances in the bladder epithelium. Photodynamic therapy induces sharply demarcated necrosis in the short post-therapy course. Laser treatment destroys the tumor, and may induce atypia in adjacent endothelial cells. Gene therapy-related changes have not been well defined yet.

Prolifération myofibroblastique pseudosarcomateuse de la vessie

Myofibroblastic proliferations of the bladder in adults are unusual lesions with a benign course. These proliferations, whether spontaneous or secondary to instrumentation, have identical morphology and behaviour. Histologically, similar lesions have been reported in the literature using different names, such as inflammatory pseudotumour, pseudosarcomatous fibromyxoid tumour, nodular fasciitis, postoperative spindle cell nodule... Recently, some authors proposed that these lesions are similar enough to be considered the same entity, designated as "pseudosarcomatous myofibroblastic proliferation" and insisted on the necessity to distinguish them from the inflammatory myofibroblastic tumour of the childhood. The latter, recently recognized as tumour, has a malignant potential and is capable of giving metastases. We describe the case of a 17-year-old man who presented a vesical mass. The histopathological study concluded to a pseudosarcomatous myofibroblastic proliferation. We discuss, through a literature review, the relationship of this lesion with inflammatory myofibroblastic tumour and its main differential diagnoses.

Tumor-like lesions of the urinary bladder

Tumor-like lesions of the urinary bladder are reviewed emphasizing those that are most diagnostically challenging for the pathologist and may result in serious errors in patient care if misinterpreted. The first category considered, pseudocarcinomatous proliferations, represents an area of bladder pathology only recently appreciated as being particularly treacherous because of the extent to which irregular islands of benign epithelial cells may seemingly penetrate the lamina propria and cause confusion with carcinoma. Somewhat orderly proliferations of this type have been known for years, von Brunn's nests, and are rarely a challenge for the experienced, but proliferations of an irregular nature such as may be seen most often as a result of prior radiation therapy, but sometimes due to chemotherapy or even ischemia, represent a challenging interpretation. The clinical history may be very important in arriving at the correct diagnosis as is the appreciation that the morphology, although architecturally problematic, is different from that of any of the familiar patterns of invasive carcinoma. Florid epithelial proliferations in fibroepithelial polyps are also briefly noted. Within the category of glandular proliferations, emphasis is placed on the wide spectrum of morphology of nephrogenic adenoma including its pseudoinfiltrative pattern and occasional propensity for tiny tubules to be misconstrued as signet-ring cells. The spectrum of müllerian glandular lesions including the relatively recently described mucinous variant, endocervicosis, is reviewed. The reactive papillary proliferation, papillary–polypoid cystitis, is then discussed. This entity has long been known but has recently been re-emphasized. Other non-neoplastic papillary lesions include florid papillary forms of nephrogenic adenoma. The past 25 years has seen a great expansion of knowledge concerning non-neoplastic spindle cell proliferations, including those related to a prior procedure, the postoperative spindle cell nodule and those without such a history, variously designated inflammatory pseudotumor, pseudosarcomatous myofibroblastic proliferation, or even other terms. The morphologic spectrum is explored and it is recommended that the two categories be retained.

Postoperative spindle cell nodule of the breast: Pseudosarcomatous myofibroblastic proliferation following endo‐surgery

Despite the frequent use of fine-needle aspiration, core biopsy and surgery, postoperative spindle cell nodule (PSCN) is a rare pathological complication that may be diagnostically treacherous. Presented herein is the case of a 52-year-old woman who developed a 7 mm mammary nodular lesion 66 days after removal of an area of columnar cell hyperplasia involving cellular and architectural atypia, performed with the Mammotome Breast Biopsy System. The lesion was highly cellular and composed of intersecting fascicles of plump spindle cells with blunt-ended elongated nuclei and nucleoli easily visible. Interspersed mononuclear cells and hemosiderin-laden macrophages were evident. PSCN is a reactive, benign myofibroblastic proliferation. Differential diagnosis includes benign and malignant spindle cell lesions of the breast. Recognition of this reactive lesion will avoid overdiagnosis of spindle cell malignant tumor. Attention to clinicopathological and histological features should result in accurate recognition of this lesion.

Soft tissue tumors of the urinary bladder, part I: myofibroblastic proliferations, benign neoplasms, and tumors of uncertain malignant potential

Most bladder tumors arise from the urothelium. However, there are several uncommon but significant bladder lesions that must be differentiated from urothelial carcinomas. These include both benign and malignant spindle cell lesions. The first half of this 2-part review will describe benign myofibroblastic proliferations including inflammatory myofibroblastic tumor and postoperative spindle cell nodule; benign neoplasms including leiomyoma, hemangioma, neurofibroma, and schwannoma; and tumors of uncertain malignant potential including paraganglioma, granular cell tumor, and perivascular epithelioid cell tumor. Common clinical presentations, morphological characteristics, and immunohistochemical features are described to aid the practicing pathologist in the identification of these entities. This review also describes current theories as to the pathogenesis of inflammatory myofibroblastic tumor and postoperative spindle cell nodule and details the current molecular markers identifying several of these lesions.

Trisomy 7 in postoperative spindle cell nodules

Postoperative spindle cell nodule is a localized, non-neoplastic, reparative lesion composed of closely packed proliferating spindle cells and capillaries simulating a leiomyosarcoma. The lesion typically develops at the site of a recent surgical wound several weeks to months postoperatively. Local recurrence of postoperative spindle cell nodules has not been reported, even after incomplete resection. We cytogenetically analyzed two postoperative spindle cell nodules, one arising in the vulva and the other in the urinary bladder. Trisomy 7 was identified as the sole karyotypic abnormality in the lesion from the vulva, in which cell culturing and G-banding analysis were possible. The other case, from the urinary bladder, showed presence of trisomy 7 by interphase-FISH performed on nuclei extracted from paraffin-embedded tissue.

Pseudosarcomatous and sarcomatous proliferations of the bladder

Pseudosarcomatous fibromyxoid tumor (PFT), postoperative spindle cell nodule (PSN), sarcoma, and sarcomatoid carcinoma of the bladder are frequently difficult to distinguish histopathologically with significant differences in disease-related outcomes. A retrospective review of our pathology registry over the last 25 years identified 7 PFT, 10 PSN, 18 primary bladder sarcomas, and 17 sarcomatoid carcinomas. Most patients with PFT, PSN, sarcoma, and sarcomatoid carcinoma were diagnosed between the ages of 50 to 60 years with PFT and PSN most commonly detected in women. A previous history of urological instrumentation and bladder cancer was present in all patients with PSN but none of the patients with PFT. Pseudosarcomatous fibromyxoid tumors were characterized by a tissue culture-like proliferation of myofibroblastic cells with focal atypia and overall cytoarchitectural features mimicking nodular fasciitis. Sarcomas and sarcomatoid carcinomas exhibited cellular atypia, mitotic activity with atypical mitosis, and the presence of necrosis. Transurethral resection was sufficient to control all PFT and PSN with no evidence of distant metastatic spread. In contrast, local recurrences and distant metastases frequently occurred in patients with primary sarcoma and sarcomatoid carcinoma despite aggressive surgical management, which was often combined with neoadjuvant chemotherapy (50% and 65% disease-specific mortality, respectively). Pseudosarcomatous fibromyxoid tumor and PSN have unique clinical and pathologic features that allow their distinction from primary bladder sarcoma and sarcomatoid carcinoma.

Inflammatory Myofibroblastic Tumors of the Urinary Tract: A Clinicopathologic Study of 46 Cases, Including a Malignant Example Inflammatory Fibrosarcoma and a Subset Associated With High-grade Urothelial Carcinoma

Inflammatory myofibroblastic tumor (IMT) of the urinary tract, also termed postoperative spindle cell nodule, inflammatory pseudotumor, and pseudosarcomatous fibromyxoid tumor, is rare and in the past was believed to reflect diverse entities. We reviewed a series of 46 IMTs arising in the ureter, bladder, and prostate, derived primarily from a large consultation practice. There were 30 male and 16 females aged 3 to 89 years (mean 53.6). Lesions were 1.2 to 12 cm (mean 4.2). There was a history of recent prior instrumentation in 8 cases. Morphology was similar to that previously described for IMT occurring in this region, with the exception of 1 case that focally appeared sarcomatous. Polypoid cystitis coexisted in 5 patients (11%). Mitoses were typically scant (0 to 20/10 hpf, mean 1). Necrosis was seen in 14 (30%) cases. Invasion of the muscularis propria was documented in 19 (41%). By immunohistochemistry (IHC), lesions at least focally expressed anaplastic lymphoma kinase (ALK) (20/35, 57%), AE1/3 (25/34, 73%), CAM5.2 (10/15, 67%), CK18 (6/6, 100%), actin (23/25, 92%), desmin (15/19, 79%), calponin (6/7, 86%), caldesmon (4/7, 57%, rare cells), p53 (10/13, 77%), and most lacked S100 (0/14), CD34 (0/13), CD117 (2/13, 15%), CD21 (0/5), and CD23 (0/3). ALK gene alterations were detected by fluorescence in situ hybridization (FISH) in 13/18 (72%) tested cases, including 2 with prior instrumentation; 13/18 (72%) showed agreement between FISH ALK results and ALK protein results by IHC. Most bladder IMTs were managed locally, but partial cystectomy was performed as the initial management in 7 cases and cystectomy in 1 (1 IMT was initially misinterpreted as carcinoma, 1 IMT was found incidentally as a separate lesion in a cystectomy specimen performed for urothelial carcinoma). Follow-up was available in 32 cases (range 3 to 120 mo; mean 33; median 24). There were 10 patients with recurrences (2 with 2 recurrences). Recurrences were unassociated with muscle invasion or with ALK alterations. In 2 cases, tumors of the urinary tract (TURs) showing IMT preceded (1 and 2 mo, respectively) TURs showing sarcomatoid carcinoma with high-grade invasive urothelial carcinoma accompanied with separate fragments of IMT. Even on re-review the IMT in these 2 cases were morphologically indistinguishable from other cases of IMT, with FISH demonstrating ALK alterations in the IMT areas in one of them. Both these patients died of their carcinomas. Lastly, there was 1 tumor with many morphological features of IMT and an ALK rearrangement, yet overtly sarcomatous. This case arose postirradiation for prostate cancer 4 years before the development of the lesion, with tumor recurrence at 4 months and death from intra-abdominal metastatic disease at 9 months. In summary, urinary tract IMTs are rare and share many features with counterparts in other sites, displaying similar morphology and immunogenotypic features whether de novo or postinstrumentation. Typical IMTs can be locally aggressive, sometimes requiring radical surgical resection, but none of our typical cases metastasized, although they can rarely arise contemporaneously with sarcomatoid urothelial carcinomas. For these reasons, close follow-up is warranted.

Pseudosarcomatous Myofibroblastic Proliferations of the Bladder

Inflammatory pseudotumor or pseudosarcomatous fibromyxoid tumor and postoperative spindle cell nodule of the bladder are unusual lesions of uncertain pathogenesis which share overlapping, if not identical, histologic features. We present our experience with 42 cases, the largest series to date, to study the etio-pathogenesis, histologic features, biologic behavior and relationship to "inflammatory myofibroblastic tumor" of childhood. Patients ranged in age from 7 to 77 years (mean 47 y) and males predominated (3.2:1). Most patients presented with hematuria (31/42). Common associations were smoking (10/30) and previous instrumentation or surgery (9/42). The clinicopathologic features of patients having or not having prior instrumentation were identical. Grossly the lesions were polypoid or nodular and involved any portion of bladder wall, most commonly the dome (9/27) and measured 1 to 10 cm (mean 4 cm). They were composed of spindled and stellate cells arranged in a myxoid background with numerous inflammatory cells. Myxoid hypocellular areas were more pronounced near the mucosal surface with greater cellularity and a fascicular arrangement in the deep aspect of the lesion. "Atypical" features included mitotic activity (0 to 20/10 HPF; mean 2/10 HPF; median 1/10 HPF; none atypical), necrosis (22/42), and extension into muscularis propria (28/32) or perivesicular fat (3/8). Lesions were positive for cytokeratin (31/33), SMA (23/34), desmin (21/35), and Alk-1 protein (12/26). FISH confirmed the Alk-1 translocation in 4/6 cases. Treatment included transurethral resection (30/42), partial cystectomy (9/42), and total cystectomy (3/42). Initial diagnostic error resulted in radiotherapy and chemotherapy in 3 patients. Follow-up was available in 28 patients. (range 3 to 93 mo; median 25 mo). Three patients developed recurrences, but none had metastases. Because the clinicopathologic features of lesions associated with and without instrumentation were similar and inseparable, we believe they are essentially the same entity, and propose the term pseudosarcomatous myofibroblastic proliferation. The preponderance of evidence which includes the extravesical growth, local recurrence, and Alk-1 gene translocation in some cases suggests perhaps a neoplastic process with limited growth potential. Even in the face of atypical histologic features (muscle invasion and necrosis) the prognosis is excellent. Despite the Alk-1 gene translocation, there continues to be sufficient evidence for regarding these as distinct from the so-called inflammatory myofibroblastic tumor of childhood.

Benign postoperative spindle cell nodule of the urinary bladder? don't think so.

According to colleagues specializing in genitourinary pathology, the so-called postoperative spindle cell nodule of the bladder can be extremely difficult to distinguish from a spindle cell sarcomatoid carcinoma. What I have learned in 25 years about spindle cell sarcomatoid carcinoma of the larynx may, by analogy, possibly help with the genitourinary pathology problem.

Nonepithelial tumor-like lesions of the prostate: a never-ending diagnostic problem.

Nonepithelial tumor-like lesions of the prostate include benign prostatic hyperplasia-associated stromal nodules, postoperative spindle cell nodules, benign mesenchymal tumors and sarcomas. These lesions and neoplasms are rare but need to be exactly classified for adequate treatment. This review focuses on the differential diagnosis between the various benign and malignant entities and compares the new WHO classification with a recently published typing of prostatic stromal lesions of unknown malignant potential.