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Ewing's sarcoma. A critical analysis of 165 cases.
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[On the problem of atypical forms of Ewing's sarcoma].
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[Ewing's sarcoma (clinical recovery with radiotherapy after 7 years)].
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[Ewing's sarcoma of 3 year's development].
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Radiotherapy of Ewing's sarcoma.
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The molecular mechanisms responsible for resistance to ET-743 (Trabectidin; Yondelis) in the Ewing's sarcoma cell line, TC-71.
Identification of new active agents against sarcoma is considered an important challenge in medical oncology. ET-743 (Trabectidin; Yondelis) has recently emerged as the first active drug developed against sarcoma in the last two decades, with promising results especially against soft-tissue sarcoma and Ewing's sarcoma (ES). In this study, we analyzed the molecular mechanisms responsible for resistance to ET-743 in ES cells. Three resistant cell variants (TC/ET 3 nM, TC/ET 6 nM and TC/ET 12 nM) were obtained, showing 28-, 47- and 102-fold increase in ET-743 resistance. Cross-resistance to other drugs was analyzed. Comparative genomic hybridization and cDNA microarray technology were employed to characterize and compare the gene expression profile of two TC/ET variants with the parental cell line. TC/ET cells show a conventional multidrug resistance phenotype and P-glycoprotein overexpression was found to significantly contribute to ET-743 resistance. However, functional studies with the cyclosporine analogue, PSC-833, indicate that other mechanisms are involved in resistance to ET-743. The gene expression profile of TC/ET cells indicated, among up-regulated genes, an increase in expression of insulin-like growth factor receptor-I (IGF-IR) and one of its major intracellular mediators, insulin receptor substrate-1. Functional studies using a neutralizing antibody anti-IGF-IR confirmed involvement of this signaling pathway in resistance to ET-743. Simultaneous blockage of both P-glycoprotein and IGF-IR completely restored sensitivity to ET-743 in ES cells. Overall, these findings provide impetus for future studies testing the therapeutic value of new specific inhibitors of P-glycoprotein and IGF-IR, which could represent a concrete therapeutic option for ES patients refractory to conventional agents.
Osteogenic sarcoma: the past, present, and future.
The term osteogenic sarcoma (osteosarcoma) is applied to malignant bone-forming tumors, identifiable by the matrix produced, though the histologic pattern may differ greatly. Ths more cellular (osteolytic) forms of the tumor have the poorer prognosis. Other prognostic factors are 1) site of the primary tumor; 2) duration of symptoms; and 3) extent of disease and tumor size. The site of tumor origin is the metaphyseal side of the epiphyseal line. The histogenesis of the tumors accounts for this distribution. Following a diagnostic biopsy, amputation of the extremities remains the treatment of choice. In selected cases, a limb-saving radical en bloc resection may surface. Radiotherapy plays a lesser but important role as adjunctive treatment, and as primary definitive treatment in certain types of bone sarcoma (Ewing sarcoma and primary reticulum cell sarcoma of bone). Until recently, chemotherapeutic agents have been used for late palliation only. Advances in treatment, however, have resulted from the application of innovative postsurgical adjuvant chemotherapy in children. The various chemotherapeutic regimens following amputation in adults and in children are discussed. In most such series of cases following amputation alone, five-year survivals have not exceeded 15-20%, with recurrent disease appearing within 18 months in fatal cases. Current studies reflect more effective regimens of adjuvant chemotherapy, with improved palliative results in metastatic osteogenic sarcoma. Although survival is much prolonged, however, many patients show a recurrence of the disease after long intervals of control, suggesting that five-year survival may not indicate a complete cure. At M.D. Anderson Hospital, th projected overall survival rate at three years is 79% of all patients with nonmetastatic disease. These results have accrued from the use of Compadri-I and Compadri-II regimens of chemotherapy. More intensive therapy may yield higher survival rates. It is known that the immunologic status of a patient definitely relates to prognosis. Although most of the investigations with immunotherapy are preliminary, emphasis is placed on improving the immune system in immunodeficient patients.
[Clinical picture of osteogenic sarcoma, osteogenic chondrosarcoma and Ewing's sarcoma].
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[Contribution to central nervous system tumor diagnosis by means of cytocentrifuged cerebrospinal fluid].
The cytocentrifugation of the liquor cerebrospinalis provides a useful diagnostic tool to differentiate benign from malign diseases of the central nervous system. The method is illustrated with liquor analyses in the field of pediatric oncology: medulloblastoma, leptomeninx sarcoma, plexuspapilloma, astrocytoma, Abt-Letterer-Siwe, ALL, reticulum cell sarcoma, Ewing sarcoma, retinoblastoma. The speed and ease of the processing, the highest possible cellular yield and the good preservation of the cellular characteristics are great advantages of this new method.
Ewing's sarcoma metastatic at diagnosis. Results and comparisons of two intergroup Ewing's sarcoma studies.
Two Pediatric Intergroup Ewing's Sarcoma studies of patients with metastatic disease (IESS-MD) have used multimodal therapy consisting of intensive combination chemotherapy and radiation therapy (XRT) to areas of gross disease detected at the time of diagnosis. In IESS-MD-I, conducted from 1975 to 1977, 53 eligible patients were entered and received the chemotherapeutic agents vincristine, Adriamycin (doxorubicin; Adria Laboratories, Columbus, OH), cyclophosphamide, and dactinomycin with concomitant XRT (VACA + XRT). In IESS-MD-II, conducted from 1980 to 1983, 69 eligible patients were entered and received 5-fluorouracil (5FU) in addition to the chemotherapeutic agents of IESS-MD-I; initial intensive chemotherapy was given and XRT was delayed until week 10 (VACA + 5FU, delayed XRT). The best response rate (complete and partial remissions combined) was 73% in IESS-MD-I and 70% in IESS-MD-II, so there was no statistical evidence of a difference in response rates (P = 0.62). The length of best response also was similar between studies (P = 0.79), with approximately 30% of the patients on both studies remaining in remission at 3 years. The percentage of patients surviving 5 years or more was 30 on the first study and 28 on the second study (P = 0.49). The major sites of relapse after a response were lung and bone, each occurring with nearly equal frequency. The age of the patient was related to both best response rate and survival: patients 10 years of age or younger had substantially higher response and survival rates than patients 11 years of age or older. The favorable prognosis for younger patients might be explained by a more favorable distribution of primary sites at diagnosis; 39% of patients 10 years of age or younger had rib primary sites, compared with only 16% for patients older than 10 years of age (P = 0.05). The frequency of life-threatening toxicity was substantially higher in IESS-MD-I (30%) than in IESS-MD-II (9%), but the frequency of fatal toxicity was similar (6% to 7%). Fatal complications included Adriamycin-induced cardiomyopathy, Pneumocystis carinii pneumonia, unspecified pneumonitis, and sepsis. The most common toxicity and complications were leukopenia and infections.
Ewing's sarcoma of bone: clinicopathologic aspects of 303 cases from the Intergroup Ewing's Sarcoma Study.
Clinicopathologic features of 303 cases of Ewing's sarcoma of bone collected by the Intergroup Ewing's Sarcoma Study group are described. Ewing's sarcoma was found to arise predominantly in the inferior segment of the skeleton in young white patients from 10 to 15 years of age. Of the several recognized histologic patterns, the filagree pattern--an organoid pattern consisting of bicellular strands of tissue separated by filmy vascular stroma--was associated with the lowest survival rates. Light microscopic evidence of cytoplasmic glycogen in tumor cells was found to be useful in but not requisite for diagnoses. The most important predictor of clinical behavior, regardless of treatment modality, was the site of primary involvement. Survival among patients with primary tumors in pelvic bones was lowest, whereas survival among patients with lesions in distal bones of the extremities was highest.
High-dose melphalan therapy for the treatment of children with refractory neuroblastoma and Ewing's sarcoma.
Neuroblastoma and Ewing's sarcoma are examples of pediatric cancers in which disseminated disease is often present at diagnosis or develops later in spite of combination therapy. The demonstration that marrow-ablative doses of chemotherapy can increase tumor cell kill, and that autologous bone marrow can be cryopreserved and reinfused into the patient to reverse such marrow ablation, has stimulated interest in this approach to refractory childhood cancers. We present results of treating eighteen patients with recurrent neuroblastoma and Ewing's sarcoma resistant to conventional therapy. We used supralethal doses of melphalan, supported by reinfusion of previously cryopreserved autologous bone marrow. Seven of 10 neuroblastoma and six of eight Ewing's sarcoma patients had complete or partial responses, lasting for a median of 6 months (neuroblastoma) and 3 months (Ewing's sarcoma). Prolonged hospitalization, pancytopenia complicated by sepsis, and reversible gastrointestinal toxicity were the major side effects. These results suggest this approach should be tested in therapeutic trials at an earlier disease stage in children who have cancers with a predictably bad prognosis.
[In vitro antitumor immune response induced by fusion of dendritic cells and Ewing's sarcoma cells].
OBJECTIVE: Human Ewing sarcoma A673 cells and human peripheral blood-derived DCs were fused to induce an antitumor activity against human EW. METHODS: EW A673 cells and human peripheral blood-derived DCs were fused with polyethylene glycol (PEG). RESULTS: Mature DCs with highly expressed surface markers (CD80, CD86, CD83 and HLA-DR) were generated in vitro and flow cytometry. It showed that the highest fusion efficiency was 23.01%. T cell proliferation assay indicated that the novel dendritomas in fused DCs/A673 cells were the most potent in activation of autologous T cell proliferation. The IFN-gamma assay showed that The IFN-gamma secretion by CTLs activated by the novel dendritomas increased more than by other stimulators. CTL assay demonstrated that the novel dendritomas induced A673 cell-specific cytotoxic responses to lyse the A673 cells in the context of MHC class I. CONCLUSION: The data indicates that fusion of tumor cells with DCs is an attractive strategy to induce tumor rejection.