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PubMed1999

Synovial sarcoma--identification of favorable and unfavorable histologic types: a Scandinavian sarcoma group study of 104 cases.

Synovial sarcoma has traditionally been regarded as a high-grade sarcoma and treated as such. Recently, specific types of poorly differentiated synovial sarcoma have been defined and shown to affect prognosis adversely. We studied 104 primary synovial sarcomas of the extremities and trunk wall without metastasis at diagnosis that were retrieved from the Scandinavian Sarcoma Group Registry (SSG) and the Swedish Cancer Registry from 1986 to 1994. Follow-up was available in all patients, median 6 (3-11) years for the survivors. There were local recurrences in 15% of patients and metastases in 33%. Histologically, the tumors were divided into favorable and unfavorable types. The favorable type had no significant cytologic atypia, and in most instances, no necrosis and a mitotic count of < 10/10 hpf. The unfavorable type included so-called poorly differentiated synovial sarcomas as well as recognizable biphasic and monophasic synovial sarcomas with prominent nuclear atypia, extreme cellularity and nuclear crowding. Designation of a tumor as having favorable vs. unfavorable histology conveyed more prognostic information than any single histologic factor. Kaplan-Meier estimates of metastasis-free survival at 5 years were 83% for patients with histologically favorable tumors and 31% for patients with histologically unfavorable tumors (95% confidence intervals 72-92% and 13-51%, respectively). These findings may influence future treatment protocols for synovial sarcoma.

Adolescent↗
PubMedDate not supplied

Expression of sarcoma-associated antigens p102 and p200 in human sarcoma cell lines.

BACKGROUND: Understanding tumor antigen expression and its correlation with the cell cycle may help in designing immunotherapy by monoclonal antibodies. Therefore, we studied the in vitro expression of sarcoma-associated antigens p102 and p200 in the G, S, and G2/M phases of sarcoma cell lines. METHODS: The expression of human cell surface sarcoma-associated antigens p102 and p200 was studied in 13 human sarcoma cell lines, using flow cytometry. RESULTS: p102 was detected by monoclonal antibody 19-24-6 in all 13 sarcoma cell lines, and p200 was detected by monoclonal antibody 29-13-17 in five of 13. p102 antigen expression was 1.4- to 3.4-fold higher (p < 0.001) than p200 expression. Although sarcoma cell lines showed a wide range of p102/p200 antigen expression, over 99% of the entire in vitro and in vivo cell population was found to be p102- and/or p200-positive. In three cell lines, p102 expression was cell cycle-dependent, with relative fluorescence intensity ranging from 13.8% to 23.9% higher at the G1 phase than at the G2/M phase. In three cell lines, the expression of p200 at the GI phase was 22.4% to 40.9% percent higher than at the G2/M phase. CONCLUSIONS: The heterogeneity and cell cycle dependence of p102/p200 antigen expression in sarcoma cells suggest that monoclonal antibodies 19-24-6 and 29-13-17 might be applied to the immunotherapy of sarcoma.

Animals↗
PubMed1984

Sarcoma growth in 15I5 x 7(2) chickens infected with avian sarcoma viruses of subgroup B or G.

A comparative study was made of sarcoma growth in 15I5 x 7(2) chickens infected in the wing web at 4 weeks of age with strains of subgroup B or G avian sarcoma viruses. Infection with sarcoma viruses of either subgroup B or G resulted in the formation of progressive wing web sarcomas at the site of inoculation. The survival times of the subgroup G virus-infected chickens were generally at least twice as great as the survival times of the subgroup B virus-infected chickens, which averaged 6-9 weeks postinoculation. At 5 weeks postinfection, a significantly higher titer of virus neutralizing antibody was detected in the subgroup G virus-infected chickens. Necropsy indicated that a high percentage of subgroup B virus-infected chickens exhibited fibrosarcomas at sites distal to the primary wing web sarcomas, whereas only a small percentage of subgroup G virus-infected chickens exhibited distal sarcomas. The results further indicated that the viral env gene is a determinant of the pattern of distal sarcoma formation.

Animals↗
PubMed1968

Production of virus by mammalian cells tranformed by Rous sarcoma and murine sarcoma viruses.

Cultured cells of mammalian tumors induced by ribonucleic acid (RNA)-containing oncogenic viruses were examined for production of virus. The cell lines were established from tumors induced in rats and hamsters with either Rous sarcoma virus (Schmidt-Ruppin or Bryan strains) or murine sarcoma virus (Moloney strain). When culture fluids from each of the cell lines were examined for transforming activity or production of progeny virus, none of the cell lines was found to be infectious. However, electron microscopic examination of the various cell lines revealed the presence of particles in the rat cells transformed by either Rous sarcoma virus or murine sarcoma virus. These particles, morphologically similar to those associated with murine leukemias, were found both in the extracellular fluid concentrates and in whole-cell preparations. In the latter, they were seen budding from the cell membranes or lying in the intercellular spaces. No viruslike particles were seen in preparations from hamster tumors. Exposure of the rat cells to (3)H-uridine resulted in the appearance of labeled particles with densities in sucrose gradients typical of virus (1.16 g/ml.). RNA of high molecular weight was extracted from these particles, and double-labeling experiments showed that this RNA sedimented at the same rate as RNA extracted from Rous sarcoma virus. None of the hamster cell lines gave radioactive peaks in the virus density range, and no extractable high molecular weight RNA was found. These studies suggest that the murine sarcoma virus produces an infection analogous to certain "defective" strains of Rous sarcoma virus, in that particles produced by infected cells have a low efficiency of infection. The control of the host cell over the production and properties of the RNA-containing tumorigenic viruses is discussed.

Animals↗
PubMed1989

Histopathology peer review of high-grade soft tissue sarcoma: the Scandinavian Sarcoma Group experience.

From 1981 to 1986, a total of 240 patients with a primary soft tissue sarcoma with malignancy grade III or IV were entered into an adjuvant chemotherapy multicenter trial conducted by the Scandinavian Sarcoma Group (SSG). Histopathologic peer review of all the specimens was performed by an expert pathology committee. The most common soft tissue sarcoma after review was malignant fibrous histiocytoma (MFH) (40%), followed by synovial sarcoma (15%), leiomyosarcoma (9%), liposarcoma (8%), and malignant Schwannoma (6%). In 25% of the cases the histologic type of sarcoma was reclassified, and in 40% of the cases the malignancy grade was changed. By survival analyses, the reclassification of malignancy grade seemed to be valid. Also, grading highly malignant soft tissue sarcoma in two grades (III and IV) increased the prognostic information. Of 164 tumors from the centers with the most reported cases (five centers with 25 to 51 tumors each), eight tumors were found to be ineligible for the adjuvant study (5%); of 76 tumors from 13 centers with few tumors (one to 16 tumors per center), 12 tumors were ineligible (16%). We conclude that histologic peer review is important in studies of soft tissue sarcoma.

Follow-Up Studies↗
PubMed1985

Radiographic appearance of Ewing sarcoma of the hands and feet: report from the Intergroup Ewing Sarcoma Study.

Review of current data from the Intergroup Ewing Sarcoma Study (IESS) shows that Ewing sarcoma is rare in bones of the hands and feet. The 12 patients from the IESS protocols with hand or foot Ewing sarcoma are comparable to those already reported in the literature. With the exception of lesions in the calcaneus, the prognosis for disease-free survival is excellent. The radiographic features of hand and foot Ewing sarcoma are generally those of classic Ewing sarcoma: permeation, soft-tissue mass, and, often, associated sclerotic reaction. However, with the exception of sclerosis, features suggesting bone reaction and slow tumor growth in these patients were distinctly uncommon compared with Ewing sarcoma in general. Those radiographic features suggesting aggressive behavior were slightly more common than in the general Ewing population. Even so, neither the radiographic appearance nor the greatest dimension of the radiographic lesion can be shown to contribute significantly to prognostication in these patients. Apparently location of the lesion is important, since in the reported cases in the literature and in this series, lesions of the calcaneus fared poorly. The importance of this set of patients therefore relates to awareness and early recognition of an unusual appearance and location of Ewing sarcoma.

Adolescent↗
PubMed1996

Body cavity-based malignant lymphoma containing Kaposi sarcoma-associated herpesvirus in an HIV-negative man with previous Kaposi sarcoma.

BACKGROUND: The role of Kaposi sarcoma-associated herpesvirus in the development of malignant lymphomas in patients negative for the human immunodeficiency virus (HIV) has not been established. OBJECTIVE: To examine the possible role of Kaposi sarcoma-associated herpesvirus in a case of body cavity-based malignant lymphoma that occurred in an HIV-negative patient who had previously had Kaposi sarcoma. DESIGN: Case study. SETTING: Academic medical center. PATIENT: A 94-year-old man with lymphomatous ascites. MEASUREMENTS: Polymerase chain reaction (PCR) and Southern blot DNA analysis. RESULTS: The body cavity-based lymphoma cells were positive for Kaposi sarcoma-associated herpesvirus by PCR and were negative for other herpesviruses, including Epstein-Barr virus, cytomegalovirus, and human herpesviruses 6 and 7. Southern blot analysis of lymphoma DNA showed high levels of Kaposi sarcoma-associated herpesvirus (> 40 to 80 genomes/cell). Clonal rearrangement of the immunoglobulin JH and JK genes was present, confirming the presence of a clonal B-cell proliferation. CONCLUSIONS: Kaposi sarcoma-associated herpesvirus may be involved in the development of malignant lymphoma after Kaposi sarcoma in HIV-negative patients. This type of lymphoma, in contrast to body cavity-based lymphoma related to the acquired immunodeficiency syndrome, may have an indolent clinical course.

Aged↗
PubMed1983

Epidermal growth factor receptor metabolism and protein kinase activity in human A431 cells infected with Snyder-Theilen feline sarcoma virus or harvey or Kirsten murine sarcoma virus.

When human A431 cells, which carry high numbers of epidermal growth factor (EGF) receptors, are exposed to EGF, the total content of phosphotyrosine in cell protein is increased, the EGF receptor becomes phosphorylated at tyrosine, and new phosphotyrosine-containing 36,000- and 81,000-dalton proteins are detected. We examined the properties of A431 cells infected with Snyder-Theilen feline sarcoma virus, whose transforming protein has associated tyrosine protein kinase activity, and Harvey and Kirsten sarcoma viruses, whose transforming proteins do not. In all cases, the infected cells were more rounded and more capable of anchorage-independent growth than the uninfected cells. EGF receptors were assayed functionally by measuring EGF binding and structurally by metabolic labeling and immunoprecipitation. In no case did infection appear to alter the rate of EGF receptor synthesis, but infection reduced EGF receptor stability by about 50% for cloned Harvey sarcoma virus-infected cells and by 80% for cloned feline sarcoma virus-infected cells. The corresponding reductions in EGF binding were 70 and 90%, respectively. The proteins of feline sarcoma virus-infected A431 cells contained an increased amount of phosphotyrosine, and the 36,000- and 81,000-dalton phosphoproteins were detected. The EGF receptor was not detectably phosphorylated at tyrosine, however, unless the cells were exposed to EGF. The Harvey and Kirsten sarcoma virus-infected cells did not exhibit elevated levels of phosphotyrosine either in the total cell proteins or in the EGF receptor, nor were the 36,000- and 81,000-dalton proteins detectable. However, these phosphoproteins were found in the infected cells after EGF treatment. Thus, all of the infected A431 cells exhibited reduced EGF binding and increased degradation of EGF receptors, yet their patterns of protein phosphorylation were distinct from those of EGF-treated A431 cells.

Autoradiography↗
PubMed2004

Kaposi sarcoma herpesvirus-induced cellular reprogramming contributes to the lymphatic endothelial gene expression in Kaposi sarcoma.

The biology of Kaposi sarcoma is poorly understood because the dominant cell type in Kaposi sarcoma lesions is not known. We show by gene expression microarrays that neoplastic cells of Kaposi sarcoma are closely related to lymphatic endothelial cells (LECs) and that Kaposi sarcoma herpesvirus (KSHV) infects both LECs and blood vascular endothelial cells (BECs) in vitro. The gene expression microarray profiles of infected LECs and BECs show that KSHV induces transcriptional reprogramming of both cell types. The lymphangiogenic molecules VEGF-D and angiopoietin-2 were elevated in the plasma of individuals with acquired immune deficiency syndrome and Kaposi sarcoma. These data show that the gene expression profile of Kaposi sarcoma resembles that of LECs, that KSHV induces a transcriptional drift in both LECs and BECs and that lymphangiogenic molecules are involved in the pathogenesis of Kaposi sarcoma.

Cell Line↗
PubMed1981

A third class of avian sarcoma viruses, defined by related transformation-specific proteins of Yamaguchi 73 and Esh sarcoma viruses.

The gag-linked transformation-specific protein (polyprotein) p80 of Esh avian sarcoma virus (ESV) has been compared by tryptic peptide mapping with the homologous protein p90 of Yamaguchi 73 avian sarcoma virus (Y73). p80 of ESV and p90 of Y73 were found to share all four of their major nonstructural, transformation-specific, methionine-containing peptides and to have at least seven cysteine-containing transformation-specific peptides in common. Two nonstructural cysteine-containing peptides unique for ESV p80 and three specific for Y73 p90 were also identified. None of these peptides were found in the transforming gene product pp60src of Rous sarcoma virus (RSV) or in the transformation-specific polyproteins p105 of avian sarcoma virus PRCII (PRCII) or p140 of Fujinami sarcoma virus (FSV). ESV p80 and Y73 p90 are phosphorylated, and their tryptic phosphopeptides appear to be identical. In each polyprotein two major phosphopeptides were demonstrated, one containing phosphoserine, the other phosphotyrosine. The latter serves as phosphoacceptor for the protein kinase activities (ATP:protein phosphotransferase, EC 2.7.1.37) associated with p80 and p90. These protein kinase activities were found to be functionally indistinguishable but could be easily distinguished from the activities associated with PRCII p105 and FSV p140 on the basis of their cation requirement and target site specificity. On that basis also, p80/p90-associated protein kinases were found to be more similar to the enzymatic activity of pp60src than to those associated with the PRCII and FSV transformation-specific polyproteins. These results document a close genetic relationship between the two independently isolated sarcoma viruses Y73 and ESV. On the basis of the relatedness of transformation-specific proteins, ESV and Y73 constitute class III of avian sarcoma viruses, with class I containing the various strains of RSV and class II encompassing FSV and PRCII.

Alpharetrovirus↗
PubMed1998

Kaposi sarcoma-associated herpesvirus/human herpesvirus 8, cytokines, growth factors and HIV in pathogenesis of Kaposi's sarcoma.

Epidemiological studies have strengthened the case for Kaposi sarcoma-associated herpesvirus/human herpesvirus 8 being the long-sought Kaposi sarcoma agent, but have also pointed to a role for other co-factors. Like other tumour viruses, Kaposi sarcoma-associated herpesvirus/human herpesvirus 8 establishes a latent (persistent) infection in Kaposi sarcoma-spindle (tumorous) cells, but can also undergo lytic replication in these and other cell types. Several latent and lytic viral genes may play a role in the pathogenesis of Kaposi's sarcoma. Although Kaposi sarcoma-associated herpesvirus/human herpesvirus 8 contains at least two genes with transforming properties, it has not yet been shown to be oncogenic in animals. This, and other studies on inflammatory/angiogenic cellular and viral cytokines as well as HIV-Tat, emphasizes the multifactorial complexity of the pathogenesis of Kaposi's sarcoma.

Journal Article↗
PubMed2003

Fine-needle aspiration of synovial sarcoma: criteria for diagnosis: retrospective reexamination of 37 cases, including ancillary diagnostics. A Scandinavian Sarcoma Group study.

The cytologic criteria of synovial sarcoma in fine-needle aspirates were defined by a retrospective examination of 37 primary tumors. Irrespective of subtype, a typical pattern at low power was found, provided the yield was rich. The typical pattern was a mixture of dispersed cells with the presence of striped nuclei and cell-tight tumor tissue fragments with irregular borders. Often a branching network of vessels was present in the fragments, imitating a true vascular tumor. Except in poorly differentiated synovial sarcomas, the tumor cells were, small to medium in size, with rounded, ovoid, or fusiform bland nuclei with inconspicuous nucleoli. In the biphasic variant, small glandular- or acinar-like structures were present, although not in all cases. In the poorly differentiated type, however, the cellular pleomorphism was marked with the presence of cells with irregular nuclei and rhabdomyoblast-like cells, corresponding to the pleomorphic variant. The Ewing's sarcoma-like and the atypical spindle cell variants of poorly differentiated synovial sarcoma were not diagnosed in the material. An unequivocal diagnosis of sarcoma is possible when the yield is rich. However, ancillary diagnostics are necessary for a correct diagnosis, to avoid important pitfalls, such as other sarcomas with bland tumor cells and vessel-rich tumor fragments, in particular, solitary fibrous tumor and true hemangiopericytoma. Electron microscopic and/or molecular genetic analyses were better diagnostic adjuncts than immunocytochemistry.

Biopsy, Fine-Needle↗
PubMed1982

Isolation of 16L virus: a rapidly transforming sarcoma virus from an avian leukosis virus-induced sarcoma.

We have isolated a replication-defective rapidly transforming sarcoma virus (designated 16L virus) from a fibro-sarcoma in a chicken infected with td107A, a transformation-defective deletion mutant of subgroup A Schmidt-Ruppin Rous sarcoma virus. 16L virus transforms fibroblasts and causes sarcomas in infected chickens within 2 wk. Its genomic RNA is 6.0 kilobases and contains sequences homologous to the transforming gene (fps) of Fujinami sarcoma virus (FSV). RNase T1 oligonucleotide analysis shows that the 5' and 3' terminal sequences of 16L virus are indistinguishable from (and presumably derived from) td107A RNA. The central part of 16L viral RNA consists of fps-related sequences. These oligonucleotides fall into four classes: (i) oligonucleotides common to the putative transforming regions of FSV and another fps-containing avian sarcoma virus, UR1; (ii) an oligonucleotide also present in FSV but not in UR1; (iii) an oligonucleotide also present in UR1 but not in FSV; and (iv) an oligonucleotide not present in either FSV, UR1, or td107A. Cells infected with 16L virus synthesize a protein of Mr 142,000 that is immunoprecipitated with anti-gag antiserum. This protein has protein kinase activity. These results suggest that 16L virus arose by recombination between td107A and the cellular fps gene.

Animals↗
PubMed1996

Primary pulmonary sarcoma with morphologic features of monophasic synovial sarcoma and chromosome translocation t(X; 18).

The authors report an unusual spindle cell sarcoma that arose in the lung of a 12-year-old girl. This tumor had histologic, immunophenotypic, and ultrastructural features consistent with monophasic fibrous synovial sarcoma. These features included a growth pattern of densely packed spindle cells in irregularly intersecting, broad fascicles, diffuse vimentin immunoreactivity, and focal expression of epithelial membrane antigen and S100 protein. This diagnosis was further supported by cytogenetic studies showing the specific t(X; 18) chromosomal translocation associated with synovial sarcoma. This balanced translocation appears to be an essentially universal characteristic of these sarcomas, regardless of histologic subtype or site of origin. The constellation of morphologic and cytogenetic findings in this case firmly establishes synovial sarcoma as a subtype of pulmonary spindle cell sarcomas. The distinctive features of these neoplasms allow them to be distinguished from a variety of primary and metastatic malignancies in the lung.

Child↗
PubMed1996

Two tumor-associated membrane antigens defined by monoclonal antibodies in a transplantable sarcoma induced by Rous sarcoma virus in rat.

Two hybridoma clones have been produced by hybridization of murine myeloma cell line PAI and splenocytes from BALB/c mice immunized with cells from a transplantable sarcoma induced in rat by SR-RSV. The antibody produced by hybridoma clone 2C2 was of subclass IgG3 and recognized a cell surface antigen of 52 kD. It only cross-reacted with cells from SR-RSV-induced sarcoma in hamster, but not with cells from the chicken RSV-induced sarcoma, nor with a number of methylcholanthrene sarcomas and various other tumors of viral or other etiology developed in rats, mouse, hamsters or chickens. The antibody produced by hybridoma clone 5G2 was of subclass IgG2A and recognized an antigen of 28 kD which was located under the plasma membrane, particularly in the cell protrusions and microvilli. Cross-reactions were found with all sarcoma cells tested, indicating that this antigen might represent a common sarcoma antigen of comparatively low molecular mass.

Animals↗
PubMed1997

Flow cytometric DNA content analysis of 185 soft tissue neoplasms indicates that S-phase fraction is a prognostic factor for sarcomas. French Federation of Cancer Centers (FNCLCC) Sarcoma Group.

BACKGROUND: The authors determined the flow cytometric (FCM) DNA characteristics of 53 benign tumors and 132 malignant (71 primary, 61 recurrent) soft tissue sarcomas to investigate their heterogeneity and to evaluate the prognostic values of DNA ploidy status and S-phase fraction (SPF). METHODS: One to 11 frozen samples were collected from 185 tumors at 10 participating centers of the French Federation of Cancer Centers (FNCLCC). All FCM analyses were performed in the same laboratory. Histologic diagnoses were collegially reviewed, and grade was assessed by the pathologists of the FNCLCC Sarcoma Group. Relationships between FCM, clinical, and pathologic data were investigated using univariate and multivariate analyses for risks of mortality and metastasis. RESULTS: All except 2 of the 53 benign lesions were DNA diploid. One schwannoma and one desmoid tumor exhibited small abnormal DNA peaks. SPF was low in all benign lesions. One-third of the sarcomas were DNA diploid, whereas two-thirds were DNA aneuploid. Relationships were found between aneuploidy and mitotic count, grade, and histologic subtype of malignant fibrous histiocytoma. DNA ploidy status did not influence the clinical outcome. Multiple sampling performed in 32 sarcomas showed both diploid and aneuploid samples in 6 tumors. Heterogeneity was related to tumor size. SPF evaluated in 85 sarcomas was related to DNA ploidy status, mitotic count, and grade. SPF > or = 4% was significantly associated with a low overall survival rate. In a multivariate analysis performed for the whole group of 132 patients, the single factors with independent prognostic value for patient mortality were disease free status after the treatment course (P < 0.0001) and SPF (P = 0.03). In the subgroup of patients who were initially free of metastases and free of tumor after the treatment course, SPF remained the only factor that significantly influenced the overall survival rate (P = 0.021). CONCLUSIONS: Despite its high failure rate, SPF is an independent factor in the prognosis of soft tissue sarcoma and should be considered when patients with a high mortality risk need to be selected for adjuvant chemotherapy.

Adolescent↗
PubMed1997

Dominant TCRB-V-J chain usage and clonal expansion of sarcoma-reactive CD4+ HLA-DR-restricted T cells suggest a limited set of immunodominant sarcoma antigens.

Tumor-reactive CD4+ T cells have been isolated from tumor patients, and their specifity but not T-cell receptor (TCR) repertoire has been analyzed. Since we have described CD4+ sarcoma-reactive T-cell clones, we now sought to determine whether the TCR repertoire of these clones provides information on the spectrum of recognized sarcoma antigens. We analyzed the TCR beta (TCRB) chain repertoire of 19 CD4+ HLA-DR-restricted T-cell clones reactive with the autologous sarcoma cell line MZ-MES-1, with HLA-DR-matched tumor cell lines of different tissue origins and B-cell blasts. We identified 7 different clonotypes, which used a limited set of TCRBV and TCRBJ segments. Although the CDR3 of the different clonotypes was diverse, repeated restimulation with sarcoma cells led to a monoclonal expansion of T cells with particular TCR clonotypes in 5/6 mixed lymphocyte tumor cell cultures (MLTC). One clonotype was found in 2 independent MLTC experiments. Sarcoma-reactive T cells were demonstrated in patient tumor-infiltrating lymphocytes (TIL) and peripheral blood mononuclear cells (PBMC) by clonotypic PCR. Our results indicate a limited number of immunodominant antigens expressed by the sarcoma cells. The junctional diversity of the TCR clonotypes shows that these antigens did not lead to extensive negative thymic selection as classical autoantigens would have. Therefore, the recognized antigens might represent cryptic autoantigens related to cellular transformation or proliferation.

Antigens, Neoplasm↗
PubMed1983

Epithelioid sarcoma of the vulva. Evidence suggesting a more aggressive behavior than extra-genital epithelioid sarcoma.

The authors describe two cases of epithelioid sarcoma of the vulva and summarize the clinical and pathologic experience with this vulvar neoplasm. Findings indicate that epithelioid sarcoma of the vulva usually occurs in the labia majora of young women, but may occur in later life. Clinically it may mimic a Bartholin's duct cyst, thus leading to inadequate treatment. Pathologic findings are characterized by sheets and nests of acidophilic, polygonal cells. Follow-up study suggests that vulvar epithelioid sarcoma behaves more aggressively than extragenital epithelioid sarcoma. Four of five patients died of metastatic sarcoma. The courses of three patients were quite rapid, whereas a fourth patient had multiple recurrences over a long period, which is typical of extragenital epithelioid sarcoma. Complete initial excision is important. All patients with local recurrence died with distant metastases. Vascular invasion also indicates a poor outcome.

Adult↗