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At least 145 records · Page 8Linked to original sources
PubMed1978

Nonproducer malignant tumor cells with rescuable sarcoma virus genome isolated from a recurrent Moloney sarcoma.

Cells from a secondary tumor developing at the site of a regressed Moloney sarcoma virus-induced tumor could be passaged in adult STU mice by intramuscular and intraperitoneal inoculation. The tumors induced by these cells, as well as by a cell line derived from it, grew progressively and led to death of the animals between 3 and 7 wk after tumor transplantation. No evidence for production of virus from these cells was obtained or for the presence of viral antigens (p30, gp69/71). From both cell variants, sarcoma virus genome could be rescued by infection with helper virus, resulting in the establishment of a cell line producing focus- and XC plaque-forming virus. The rescued producer cells very frequently also produced tumors which finally grew progressively. The nonproducer cells were not immunogenic, as was demonstrated in cross transplantation tests and in studies for cell-mediated cytotoxicity (CMC) and complement-dependent antibody-mediated cytotoxicity (AMC). The producer cells, however, were demonstrated to possess a strong immunogenicity. The nonproducer cells, though nonimmunogenic, revealed a weak immunosensitivity when used for challenge in the transplantation protection assay or as target cell for the demonstration of AMC and CMC, if the immune response was induced by cells producing the sarcoma-helper virus complex, but not by cells producing only helper virus. The nonproducer cells, as well as their rescued producer derivative, showed a stronger reactivity with cytotoxic antibodies than with cytotoxic cells, whereas the helper virus-producing cell line was comparably suitable as target cell for AMC and CMC. The recurrence of a regressed Moloney sarcoma is assumed to be the result of the occurrence of transformed nonproducer cells escaping immune destruction, and not as a consequence of a depleted immune resistance in the host.

Animals↗
PubMed1982

Fusion injection of Rous Sarcoma virus proteins into Rous sarcoma virus-transformed, non-producing hamster cells causes release of infectious virus.

Purified virus proteins from transformation-defective (td) mutants of Rous sarcoma virus PrA or PrB were trapped in human erythrocyte ghosts which, after resealing, were fusion-injected into hamster RBH cells or rat TWERC cells. These cell lines are non-productively transformed by subgroup C Rous sarcoma virus. After fusion injection the hamster RBH cells released transforming subgroup C Rous sarcoma virus. No infectious virus could be rescued from rat TWERC cells. Since previous experiments have shown that fusion injection of the purified Rous sarcoma virus protein p15 into hamster RBH cells caused cleavage of the precursor protein pr76 to form the virus group-specific antigen (gag) but did not induce infectious virus, we conclude that in addition to p15 other virus proteins are required to induce virus rescue in hamster RBH cells.

Animals↗
PubMed1970

Microcytotoxicity test: detection in sarcoma patients of antibody cytotoxic to human sarcoma cells.

A microcytotoxicity test has been used to detect a factor cytotoxic for human sarcoma cells; the factor was found in serums from 70 percent of sarcoma patients, 58 percent of their family members, and 8 percent of serums from normal blood donors. This cytotoxin is an antibody against a common cell surface sarcoma antigen since it is specific for sarcoma cells, is complement dependent, and is extractable with the globulin fraction of serum.

Antibodies↗
PubMed1972

Reversion of murine sarcoma virus transformed mouse cells: variants without a rescuable sarcoma virus.

Murine sarcoma virus transformed mouse 3T3 cells, which are negative for murine leukemia virus and which yield sarcoma virus after superinfection with murine leukenmia virus, spotaneously give rise to flat variants front which murine sarcoma virus can no longer be rescued. The revertants support leukemia viruis growth and show an enhanced sensitivity to murine sarcoma superinfection and, like normal cells, do not release RNA-dependent DNA polymerase activity. Because revertants could be obtained with high frequency from progeny of single transformed cells, each cell that containts the sarconma virus genome seems to have the capacity to suppress or eliminate an RNA tumor virus native to its species of origin.

Animals↗
PubMed1973

Transformation of rat liver cells with chicken sarcoma virus B77 and murine sarcoma virus.

Rat liver cells in vitro were transformed with chicken sarcoma virus B77, giving RL(B77) cells, and with murine sarcoma virus (Harvey), giving RL(MSV) cells. Rat liver cells transformed spontaneously in vitro were designated RL cells. In addition, the RL(MSV) cell line was adapted for growth in culture fluid containing 25 mug of 5-bromodeoxyuridine per ml. All cell lines were tumorigenic in 1-wk-old rats. The number of cells needed for induction of tumor growth was 1,000-fold higher in the case of RL(B77) cells in comparison with RL(MSV) cells and RL cells. No production of viral particles from any of the cell lines investigated was detected by plating concentrated supernatant fluid of the cultures on different secondary embryo cells with and without fusion by Sendai virus, by labeling with uridine-5-(3)H, or by assay for deoxyribonucleic acid polymerase activity. The viral genome was rescued by fusion of RL(B77) cells with chicken cells. Chicken sarcoma virus rescued from (RL(B77) cells differed in plating efficiency on duck cells from B77 virus rescued from transformed rat embryo cells. No virus was rescued after fusion of RL(MSV) and RL cells with mouse, rat, or chicken embryo cells. Infectious murine sarcoma virus can be induced by 5-bromodeoxyuridine from RL(MSV) cells.

Alpharetrovirus↗
PubMed1986

Phosphorylation of the transforming protein of Rous sarcoma virus: direct demonstration of phosphorylation of serine 17 and identification of an additional site of tyrosine phosphorylation in p60v-src of Prague Rous sarcoma virus.

We provide direct evidence that serine 17 is the major site of serine phosphorylation in p60v-src, the transforming protein of Rous sarcoma virus, and in its cellular homolog, p60c-src. The amino acid composition of the tryptic peptide containing the major site of serine phosphorylation in p60v-src was deduced by peptide map analysis of the protein labeled biosynthetically with a variety of radioactive amino acids. Manual Edman degradation revealed that the phosphorylated serine in this peptide was the amino terminal residue. These data are consistent only with the phosphorylation of serine 17. The major site of serine phosphorylation in chicken p60c-src, the cellular homolog of p60v-src, is contained in a tryptic peptide identical to that containing serine 17 in p60v-src of Schmidt Ruppin Rous sarcoma virus of subgroup A. Serine 17 is therefore also phosphorylated in p60c-src. The p60v-src protein encoded by Prague Rous sarcoma virus was found to contain two sites of tyrosine phosphorylation. The previously unrecognized site of tyrosine phosphorylation may be tyrosine 205 or possibly tyrosine 208. Treatment of Prague Rous sarcoma virus-infected cells with vanadyl ions stimulated the protein kinase activity of p60v-src and increased the phosphorylation of tyrosine 416 but not the phosphorylation of the additional site of tyrosine phosphorylation.

Amino Acid Sequence↗
PubMed2005

Gene expression profiling of human sarcomas: insights into sarcoma biology.

Sarcomas are a biologically complex group of tumors of mesenchymal origin. By using gene expression microarray analysis, we aimed to find clues into the cellular differentiation and oncogenic pathways active in these tumors as well as potential biomarkers and therapeutic targets. We examined 181 tumors representing 16 classes of human bone and soft tissue sarcomas on a 12,601-feature cDNA microarray. Remarkably, 2,766 probes differentially expressed across this sample set clearly delineated the various tumor classes. Several genes of potential biological and therapeutic interest were associated with each sarcoma type, including specific tyrosine kinases, transcription factors, and homeobox genes. We also identified subgroups of tumors within the liposarcomas, leiomyosarcomas, and malignant fibrous histiocytomas. We found significant gene ontology correlates for each tumor group and identified similarity to normal tissues by Gene Set Enrichment Analysis. Mutation analysis done on 275 tumor samples revealed that the high expression of epidermal growth factor receptor (EGFR) in certain tumors was not associated with gene mutations. Finally, to further the investigation of human sarcoma biology, we have created an online, publicly available, searchable database housing the data from the gene expression profiles of these tumors (http://watson.nhgri.nih.gov/sarcoma), allowing the user to interactively explore this data set in depth.

Cluster Analysis↗
PubMed1995

Doxorubicin versus CYVADIC versus doxorubicin plus ifosfamide in first-line treatment of advanced soft tissue sarcomas: a randomized study of the European Organization for Research and Treatment of Cancer Soft Tissue and Bone Sarcoma Group.

PURPOSE: The aim of this trial was to compare the activity and toxicity of single-agent doxorubicin with that of two multidrug regimens in the treatment of patients with adult advanced soft tissue sarcomas. PATIENTS AND METHODS: This was a prospective randomized phase III trial performed by 35 cancer centers within the Soft Tissue and Bone Sarcoma Group of the European Organization for Research and Treatment of Cancer (EORTC). Six hundred sixty-three eligible patients were randomly allocated to receive either doxorubicin 75 mg/m2 (arm A), cyclophosphamide, vincristine, doxorubicin, and dacarbazine (CYVADIC) (arm B), or ifosfamide 5 g/m2 plus doxorubicin 50 mg/m2 (arm C). RESULTS: The overall response rate was 24% (95% confidence interval, 20.7% to 27.3%) among eligible patients and 26% among assessable patients. No statistically significant difference was detected among the three study arms in terms of response rate (arm A, 23.3%; arm B, 28.4%; and arm C, 28.1%), remission duration (median, 46 weeks on arm A, 48 weeks on arm B, and 44 weeks on arm C), or overall survival (median, 52 weeks on arm A, 51 weeks on arm B, and 55 weeks on arm C). The degree of myelosuppression was significantly greater for the combination of ifosfamide and doxorubicin than for the other two regimens. Cardiotoxicity was also more frequent in this arm, but other toxicities were similar. CONCLUSION: In advanced soft tissue sarcomas of adults, single-agent doxorubicin is still the standard chemotherapy against which more intensive or new drug treatments should be compared. Combination chemotherapy cannot be recommended outside a controlled clinical trial with the exclusion of some subsets of sarcoma patients for whom significant tumor volume reduction may be an important end point of a chemotherapy regimen.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1998

High-dose induction chemoradiotherapy followed by autologous bone marrow transplantation as consolidation therapy in rhabdomyosarcoma, extraosseous Ewing's sarcoma, and undifferentiated sarcoma.

PURPOSE: To improve response and survival rates in patients with high-risk rhabdomyosarcoma (RMS), extraosseous Ewing's sarcoma, and undifferentiated sarcoma, we used a short course of induction with multi-agent chemotherapy, hyperfractionated radiotherapy, and surgery when possible. Consolidation was with intensive chemotherapy and autologous bone marrow transplantation (ABMT). PATIENTS AND METHODS: Twenty-six patients (21 with RMS, three with undifferentiated sarcoma, and two with extraosseous Ewing's sarcoma) were entered onto the protocol between June 1990 and March 1994. Induction consisted of ifosfamide, etoposide, doxorubicin, dactinomycin, cyclophosphomide, and vincristine, and a split course of hyperfractionated radiotherapy. Patients who attained a complete response (CR) or good partial response (GPR) received consolidation with high-dose melphalan and etoposide followed by ABMT. RESULTS: Of 26 previously untreated patients 19 (73%) achieved a CR (n=13) or GPR (n=6) at the completion of induction and underwent ABMT. Two-year overall survival (OS) was 56% (95% confidence interval [CI], 36% to 76%) and progression-free survival (PFS) was 53% for the whole group (95% CI, 33% to 73%). CONCLUSION: Consolidation of response by myeloablative chemotherapy was well tolerated. Split-course hyperfractionated radiotherapy did not increase the rate of local control. The results of this short-course therapy were comparable to previous therapies of 1 to 2 years' duration. Induction and consolidation chemotherapy, as well as radiation dose, could be further intensified, since no death due to toxicity occurred among these patients.

Adolescent↗
PubMed2005

Phase II study of ET-743 in advanced soft tissue sarcomas: a European Organisation for the Research and Treatment of Cancer (EORTC) soft tissue and bone sarcoma group trial.

PURPOSE: This nonrandomized multicenter phase II study was performed to evaluate the activity and safety of Ecteinascidin (ET-743) administered at a dose of 1.5 mg/m(2) as a 24-hour continuous infusion every 3 weeks in patients with pretreated advanced soft tissue sarcoma. PATIENTS AND METHODS: Patients with documented progressive advanced soft tissue sarcoma received ET-743 as second- or third-line chemotherapy. Antitumor activity was evaluated every 6 weeks until progression, excessive toxicity, or patient refusal. RESULTS: One hundred four patients from eight European institutions were included in the study (March 1999 to November 2000). A total of 410 cycles were administered in 99 assessable patients. Toxicity mainly involved reversible grade 3 to 4 asymptomatic elevation of transaminases in 40% of patients, and grade 3 to 4 neutropenia was observed in 52% of patients. There were eight partial responses (PR; objective regression rate, 8%), 45 no change (NC; > 6 months in 26% of patients), and 39 progressive disease. A progression arrest rate (PR + NC) of 56% was observed in leiomyosarcoma and 61% in synovialosarcoma. The median duration of the time to progression was 105 days, and the 6-month progression-free survival was 29%. The median duration of survival was 9.2 months. CONCLUSION: ET-743 seems to be a promising active agent in advanced soft tissue sarcoma, with no cumulative toxicities. The 6-months progression-free survival observed in advanced soft tissue sarcoma compares favorably with those obtained with other active drugs tested in second-line chemotherapy in previous European Organisation for the Research and Treatment of Cancer trials. The median overall survival was unusually long in these heavily pretreated patients mainly due to the high number of patients who benefit from the drug in terms of tumor control.

Adolescent↗
PubMed1975

Sarcoma-negative leukemia-positive transformed cell culture established from a murine sarcoma virus-induced rat bone tumor.

Inoculation of the Soehner-Dmochowski isolate of the Moloney strain of murine sarcoma virus (MSV), designated MSV-SD, consistently leads to the development of bone tumors in the susceptible New Zealand black (NB) rats. Two separate cell cultures have been established from 2 individual MSV-SD-induced NB rat bone tumors. Cells of 1 bone tumor culture, designated RBT-E, are in early in vitro passages. These cells form colonies in agar medium and take up 2-deoxy-D-[3H]glucose at a greatly enhanced rate, 5 times that of normal nontransformed rat embryo cells. Cells of the RBT-E culture release both MSV and murine leukemia virus (MuLV) and therefore contain sarcoma-positive leukemia-positive transformed cells. The other rat bone tumor culture, designated RBT-L, produced MSV at early passages. RBT-L culture has been passaged over 130 times in vitro. Cells of the RBT-L culture form colonies in agar medium and take up 2-deoxy-D-[3H]glucose at an enhanced rate (3 times that of rat embryo cells), indicating the presence of transformed cells within the RBT-L culture. However, cells of the RBT-L culture at late passages (Passage 130 or more) produce only MuLV and no detectable MSV activity (as shown by the lack of tumor-inducing activity and the lack of focus-forming activities by direct assay or by infectious center assay). Attempts to rescue MSV activity from RBT-L cells by cocultivation with MuLV-producing mouse cells were not successful. The MuLV found in the RBT-L cells, however, is a competent helper virus capable of rescuing the MSV genome from MSV-SD-induced hamster bone tumor cells. All the available evidence supports the notion that late passages of the RBT-L culture contain transformed cells that do not produce conventionally detectable MSV. These cells are referred to as sarcoma-negative leukemia-positive cells. The sarcoma-negative leukemia-positive cells represent a different kind of MSV-induced transformed cells and provide a unique system for studies in search of MSV markers such as MSV-specific antigens and MSV-specific nucleotide sequences.

Animals↗
PubMed1985

Simultaneous occurrence of Pneumocystis carinii pneumonia, cytomegalovirus infection, Kaposi's sarcoma, and B-immunoblastic sarcoma in a homosexual man.

The most common manifestations of the acquired immunodeficiency syndrome include Pneumocystis carinii pneumonia and/or Kaposi's sarcoma. High-grade B-cell lymphomas have also been reported in homosexual men at risk for the acquired immunodeficiency syndrome. We herein present the case of a homosexual man, who presented simultaneously with Pneumocystis carinii pneumonia, acute cytomegalovirus infection, Kaposi's sarcoma, and B-cell immunoblastic sarcoma. Severe compromise of both the B- and T-cell arms of the immune system was documented. The patient had evidence of exposure to the human T-lymphotropic retrovirus III, evidence of reactivation of Epstein-Barr virus infection, and cytomegalovirus inclusions within Kaposi's sarcoma tissue. We conclude that exposure to these viral agents in the setting of severe immunocompromise may have led to the observed "opportunistic" neoplasms.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Cellular immune response to human sarcomas: cytotoxic T cell clones reactive with autologous sarcomas. I. Development, phenotype, and specificity.

Human T cell clones cytotoxic for autologous sarcoma cell lines have been developed from patient JM with an osteogenic sarcoma, and from patients EG and RM with malignant fibrohistiocytoma. These clones were derived from the cocultivation of peripheral blood lymphocytes (PBL) with the respective patient's autologous irradiated established tumor cell lines (AIT). After two cycles of stimulation for 5 days in bulk culture, these "educated" lymphocytes were seeded at a density of 1 X 10(6) cells/well in 24-well plates and were cultured in the presence of highly purified natural IL 2 and AIT, the latter serving as a feeder layer. Cell numbers were reduced from the initial seeding density by one log each week until reaching a density of 10(2) cells. These cells were found to be stable in viability and cytotoxic activity, after which limiting dilution was then performed. Within 4 to 6 wk, clones were isolated with unique specificities. These clones were capable of proliferating to a total density of 10(9) cells/ml and maintained their specific cytotoxicity for more than 6 mo. Testing with a panel of target cells of various histotypes, cold-target inhibition assays, and blocking of cytotoxicity with anti-HLA monoclonal antibodies showed that the T cell clones recognize a common sarcoma-associated antigen and that the lysis is HLA restricted. Phenotypically, cytotoxic clones derived from JM were Leu-1+, Leu-2+, and Leu-3-, whereas those derived from EG exhibited either Leu-24 or Leu-3+ markers, the latter phenotype lacking cytotoxicity. RM exhibited mainly Leu-3+ clones with strong cytotoxicity. All were HNK-1- and HLA class II+, with less than 1% of cells of each clone stained by anti-TAC monoclonal antibody. The clones from each patient did not lyse autologous or allogeneic PBL, mitogen-induced T lymphoblasts, normal fibroblasts, cells isolated from benign neoplasms, carcinoma cells, Daudi B lymphoid cells, or K562 cells. With the exception of EG, all clones produced immune interferon in a range from 12 to 50 U/ml. The generation of long-term specific T cell clones can be used to further dissect the cellular immune response to sarcomas. Cytotoxic T cell clones have potential application for tumor immunotherapy.

Antigens, Neoplasm↗
PubMed1984

[Soft tissue clear cell sarcomas. Reevaluation of clear cell sarcomas of the tendons and the aponeuroses in 14 cases].

A retrospective study is realized including 14 cases of clear cell sarcomas of tendons and aponeuroses, found in the files of Institut Gustave-Roussy (1969-1983). The main microscopic features are emphasized. In comparison with other soft tissue sarcomas, clear cell sarcomas are clinically characterized by a great frequency of local lymph node metastases (4 of 14 cases). The prognosis is usually particularly poor. The exact histogenesis remains obscure, but the results of special stains, support origin from migrated neural crest cells: melanin is visualized in 2 out of 12 tumors in which Fontana-Masson is performed. S 100 protein, a neuroectodermal marker, is positive by immunoperoxidase technique (PAP) in 6 of 10 tested cases. A better diagnostic approach is allowed with the help of ultrastructural study performed in 3 cases. These tumors must be separated from synovialosarcomas. Because the histogenesis is not actually sure, it is preferable to call them "soft tissue clear cell sarcomas".

Adolescent↗
PubMedDate not supplied

[Clinical, radiological and pathological study of Ewing's sarcoma of the lumbar spine. Round cell sarcomas. Report on three cases (author's transl)].

Two cases of primary bone condensation type Ewing's sarcoma of a lumbar vertebra are described in children aged 8 and 10 years, as well as one case of the osteolytic form in a 14-year-old child. Ewing's sarcoma very rarely occurs in the spine, and the type with bone condensation is almost exclusively of a primary nature. The tumour extends simultaneously into the epidural space and the perispinal planes. Intravenous urography and myelography with metrizamide are therefore essential for evaluating the degree of tumour extension. Computed tomography examinations are also now necessary. Prognosis is bad and current therapeutic possibilities limited. Histological diagnosis is the only means of distinguishing Ewing's sarcoma from other round cell sarcomas in or around the spine.

Adolescent↗
PubMed1976

[The prognosis of female genital sarcomas of the adult woman with special reference to sarcomas of the uterine corpus (author's transl)].

Report on 88 cases of sarcomas of the female genital organs. The sarcomas were confined to the uterine body in 72 cases. The prognosis of this disease depends primarily on the adequacy of the treatment. The treatment consists of as radical an operation as possible followed by external radiation and intra-vaginal application of radium. The microscopic type of the sarcoma of the uterus is of secondary importance. Patients who survived for 3 years following this treatment have a good prognosis for a 5 year or a 10 year cure. Other sarcomas of the female genital tract are mentioned.

Adult↗
PubMed1973

Studies on the nucleic acid sequences of Kirsten sarcoma virus: a model for formation of a mammalian RNA-containing sarcoma virus.

The genetic information contained in the Kirsten and Moloney strains of mammalian RNA-containing sarcoma viruses has been analyzed by RNA . (3)H-DNA hybridization. Kirsten sarcoma virus has been found to possess two distinct sets of nucleic acid sequences. One set of sequences is contained in murine type C helper virus, and the other set is contained in rat type C helper virus. Moloney sarcoma virus contains sequences of murine type C helper virus but not of rat type C helper virus. The results indicate that Kirsten sarcoma virus arose through a process of recombination between Kirsten murine leukemia virus and nucleic acid sequences found in rat cells. A model is suggested for the formation of transforming type C viruses involving the transduction of oncogenic information.

Animals↗
PubMed2000

Biphenotypic sarcoma with characteristics of both a Ewing sarcoma and a desmoplastic small round cell tumor.

BACKGROUND: The EWS gene, a transcription factor of unknown function, is involved in chromosomal translocations associated with a wide variety of tumors, particularly small round blue cell tumors such as Ewing sarcoma. It has previously been reported that desmoplastic small round blue cell tumor (DSRBCT) frequently has an associated t(11;22) abnormality resulting from fusion of the EWS and WT-1 genes. PROCEDURE: We report a case of a small round blue cell tumor with characteristics of both Ewing sarcoma and DSRBCT with a t(11;22) translocation leading to fusion of the EWS and FLI1genes. RESULTS: The translocation point and fusion products were confirmed by polymerase chain reaction amplification and restriction fragment mapping of the products. CONCLUSIONS: The biphenotypic nature of this case and the apparent promiscuity of the EWS gene in tumor-associated translocations coupled with other reports of biphenotypic childhood sarcomas has potential implications for the relationship between small round blue cell tumors and the mechanism of EWS/FLI1 oncogenesis.

Carcinoma, Small Cell↗