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A well documented case of extraskeletal Ewing's sarcoma arising in a finger of a 16-year-old man was studied by light microscopy, immunohistochemistry and electron microscopy. The differential diagnoses of similar "round cell neoplasms" are discussed. Emphasis is placed on the distinction between extraskeletal Ewing's sarcoma and peripheral neuroepithelioma.
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The histogenesis of Ewing's sarcoma remains unknown. Recent studies have suggested a relationship to an unusual form of childhood neural tumor, often termed peripheral neuroepithelioma or primitive neuroectodermal tumor. Five Ewing's sarcoma tumor cell lines were studied for evidence of a neural phenotype. Under normal culture conditions, no morphologic evidence of neural differentiation was detected. Treatment with retinoic acid, an agent known to induce marked neural differentiation in neuroblastoma, had no demonstrable effect. Treatment with either cyclic AMP or TPA, in contrast, induced pronounced morphologic evidence of neural differentiation. Cells developed elongate processes with varicosities by phase-contrast microscopy; filaments, microtubules, and uraniffin-positive dense core granules were present by electron microscopy. Three neural markers (NSE, NFTP, and cholinesterase) were absent or barely detectable in untreated cells, but became abundant after treatment. These results provide convincing evidence for a neural histogenesis of Ewing's sarcoma. They also suggest a close relationship between Ewing's sarcoma and peripheral neural tumors, including the chest wall tumor described by Askin, but only a distant relationship to neuroblastoma.
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The eleventh cytogenetically analyzed Askin's tumour, diagnosed in a two-year-old girl, is reported. Chromosomal analysis revealed a pseudodiploid karyotype of tumour cells with translocations of t(11;22)(q24;q12) and der(4)t(2;4)(q24;q35). The observed t(11;22)(q24;q12) is not only a unique characteristic of all cytogenetically analyzed Askin's tumours but it also occurs in 92-100% of peripheral neuroepithelioma and of Ewing's sarcoma, irrespective of its osseous or extraosseous localization. This genetical similarity further supports a nosological concept according to which Askin's tumour, Ewing's sarcoma and peripheral neuroepithelioma represent phenotypic variations of the same tumour, namely the peripheral primitive neuroectodermal tumour.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
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We report a case of schwannoma (neurilemmoma) predominantly composed of small cells arranged in rosettes around central collagenous cores and discuss the differential diagnosis of this unusual variant. Schwannoma with giant rosettes, previously designated as neuroblastoma-like schwannoma by Goldblum et al., must be differentiated from neuroblastoma, peripheral neuroectodermal tumors, and malignant change in a schwannoma.
Malignancies of childhood include a well-defined spectrum of hematolymphoid, organ specific (adrenal, kidney, liver), soft tissue, bone, and nervous system (central and peripheral) neoplasms with variable biology. Small round cell neoplasms, a subset of childhood malignancies, are histologically similar but differ markedly in their histogenesis, therapy, and prognosis. Traditionally, clinical information and light microscopy, with the aid of histochemistry and ultrastructural evaluation, establish a diagnosis or at least narrow the differential diagnosis. Additionally, immunohistology, cytogenetics, and molecular studies have become important in diagnosis and in defining phenotype/genotype, patient treatment modalities, and prognosis in specific cases. The 11;22 chromosomal translocation typifies Ewing's sarcoma, primitive neuroectodermal tumor, and Askin's tumor, as does the resultant chimeric transcript, while expression and amplification of N-myc oncogene are predictive of the prognosis in neuroblastoma. Furthermore, studies of genes and gene products are elucidating mechanisms of oncogenesis and tumor progression.
A case of esthesioneuroblastoma, the pathological diagnosis of which almost always causes great difficulties, was investigated ultrastructurally, biochemically, and immunohistologically, using antibodies against the five known types of intermediate filaments [keratin, vimentin, desmin, glial fibrillary acidic protein (GFAP) and neurofilaments]. The tumour cells did not react with antibodies against any of the five intermediate filament proteins. Ultrastructural investigations showed dense cored secretory granules in the cytoplasm and cell processes. Thus, immunohistology offers by "exclusion" a differential diagnosis to avoid often misdiagnosed tumours (undifferentiated carcinomas, embryonal rhabdomyosarcomas, and malignant lymphomas), since carcinomas react with antikeratin, embryonal rhabdomyosarcomas with antibodies to desmin and malignant lymphomas show immunofluorescence with antibodies to vimentin. The biological behaviour (age distribution, tendency to metastasize), the normal values of biochemical parameters, homovanillic acid and vanilmandelic acid (HVA, VMA), and the absence of neurofilaments distinguish this type of tumour from the peripheral sympathetic neuroblastoma.
A 30-year-old man with peripheral neuroepithelioma which was present in the retroperitoneum underwent surgical treatment under the diagnosis of germ cell tumor. Subsequently he died of local recurrence and multiple metastases to the liver seven months after surgery. To our knowledge, this is the second case of peripheral neuroepithelioma which was observed in the retroperitoneal space in the literature of the world. We also reviewed 20 cases of peripheral neuroepithelioma reported in Japan.