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PubMedDate not supplied

Monoclonal antibody characterization of sarcoma-associated antigen p102.

A membrane protein of Mr 102,000 Da (p102) was detected in 51 out of 53 human sarcomas, using a murine IgG1 monoclonal antibody 23-26. Antigen expression in sarcoma histologic subtypes appeared dependent on the amount of fibrous tissue matrix present in the original specimen. High levels of p102 antigen were also found in all sarcoma, carcinoma cell lines and neonatal skin fibroblasts tested. Low levels of p102 were also expressed in membranes from some specimens of melanoma, lung and colorectal carcinoma, first trimester fetus, fat, lung and liver while skin specimens expressed slightly higher levels of antigen. Lectin affinity absorption indicated p102 was mannose containing glycoprotein, isoelectric point (pI) 4.7 and affinity constant of 2.3 x 10(9) M-1, with 5.9 x 10(5) binding sites per cultured human HT-1080 fibrosarcoma cell. The overexpression of p102 in sarcomas and other neoplastic tissues suggests that this protein may be associated with the neoplastic state.

Adult↗
PubMed1975

Origin and partial characterization of Fc receptor-bearing cells found within experimental carcinomas and sarcomas.

A variety of murine connective and epithelial tissue tumors, including the SAD/2 and FS9 fibrosarcomas, the TA3/Ha and CAD/2 mammary carcinomas and a primary methylcholanthrene-induced sarcoma, were found to contain a high proportion of cells with receptors for the Fc portion of immunoglobulin G ("Fc receptors"). Experiments were undertaken to assess whether these cells were neoplastic, or whether they represented the infiltration into the tumor of non-malignant host cells such as macrophages or lymphocytes. It was found that long-term established in vitro cell lines of the TA3/Ha SAD/2 and CAD/2 tumors were entirely negative for the Fc receptor, whereas injection of these cells led to the formation of tumors containing a high proportion of Fc receptor-bearing cells. Many of these cells were actively phagocytic as assessed by ingestion of iron filings or antibody-coated erythrocytes. Injection of Fc receptor-negative cultured tumor cells into F1 hybrids, in which host cells could be distinguished from the tumor cells by anti-H2 sera, revealed that many or all of the Fc receptor-bearing cells in the resultant tumor were of host origin. In contrast to its effect on normal spleen cells, anti-theta serum treatment also partially inhibited Fc rosettes, suggesting a T-lymphocyte origin for some of the Fc receptor-bearing cells. Since almost all cells with potential anti-tumor activity bear Fc receptors, it is suggested that an index of host cell infiltration of carcinomas and sarcomas can quickly and easily be ascertained by enumeration of Fc receptor-bearing cells.

Animals↗
PubMed1996

Fibrosarcoma of the thigh. Case report and literature review.

Sarcomas of the soft tissue constitute a fairly rare group of neoplasms localized mainly at the level of the extremities. Apart from clinical and semeiotic investigations, diagnosis is based on imaging techniques. Among these (ultrasound, CT, NMR and angiography), all of which are helpful in diagnosis, NMR seems to provide the most complete data and sensitivity and specificity. In fact, it has greater specificity than ultrasound or CT as regards identification of any infiltration of the muscle or deep interstitial tissues and can also contribute information on the nature of the sarcoma, as it provides high definition of the structural composition of the tissues. Angiography remains important as a preoperative guide to the surgical approach. Surgery is the treatment of choice, although in recent years it has been integrated with radio or chemotherapy. Thanks to the progress in treatment constituted by combination treatments there has been a dramatic reduction in the need for amputations, compartmental excision and disinsertion of muscle groups. We report the case of a patient with fibrosarcoma of the thigh and discuss the various imaging techniques and different approaches to the treatment of these neoplasms.

Adult↗
PubMed1978

Cardiac fibrosarcoma with bone metastases.

The diagnosis of a primary cardiac sarcoma with bone metastases was suspected in a previously normal patient because of the development of unremitting pulmonary edema and lytic bone lesions. Echocardiography substantiated the diagnosis, which proved at autopsy to be a primary fibrosarcoma of the heart. This represents only the third such case reported with bone metastases.

Bone Neoplasms↗
PubMed2005

Radiation-induced sarcoma: a challenge for the surgeon.

BACKGROUND: Treatment of radiation-induced sarcoma (RIS) remains an unsolved problem. To provide more insight into the disease process, its characteristics, outcome, and potential outcome determinants were defined. METHODS: From 1978 to 2003, 27 patients--20 females (74%) and 7 males (26%) with a median age 44 years (range, 1-73 years) at the time of diagnosis of the primary tumor--developed an RIS after a median interval of 8 years (range, 3-41 years). The histology of the RIS was 10 (37%) undifferentiated high-grade pleomorphic sarcomas, 7 (26%) angiosarcomas, 6 (22%) fibrosarcomas, 2 (7%) osteosarcomas, 1 (4%) pleomorphic rhabdomyosarcoma, and 1 (4%) pleomorphic leiomyosarcoma. Surgical resection was performed in 21 patients: 13 (62%) R0 (microscopically radical), 4 (19%) R1 (microscopically irradical), 2 (9.5%) R2 (macroscopically irradical), and 2 (9.5%) RX (unknown radicality). Six (22%) patients underwent no resection. RESULTS: The 5-year disease-free and overall survival rates were 27% and 30%, respectively. The local failure rate after R0 resection was 54%. The distant failure rate for the entire group was 41%. Patients with an R0 resection had a significantly better survival rate (P < .05) than patients with an R1, R2, or no resection. CONCLUSIONS: RISs are aggressive malignancies with a high tendency for local recurrence and distant metastases. Previously applied treatment often hampers adequate resection. Therefore, radical surgical resection is the only chance to improve disease-free and overall survival, but it may also have a palliative role. Still, the overall prognosis remains poor.

Adolescent↗
PubMed2001

Are myogenin and myoD1 expression specific for rhabdomyosarcoma? A study of 150 cases, with emphasis on spindle cell mimics.

Rhabdomyosarcoma (RMS), the most common soft tissue sarcoma of childhood, displays a variety of histologic patterns. Immunohistochemistry is used extensively to distinguish RMS from its mimics. Myogenin and MyoD1, myogenic transcriptional regulatory proteins expressed early in skeletal muscle differentiation, are considered sensitive and specific markers for RMS and are more specific than desmin and muscle-specific actin and more sensitive than myoglobin. Previous studies have focused on expression of myogenin and MyoD1 in small round cell tumors. This study assesses myogenin and MyoD1 in rhabdomyosarcoma subtypes and spindle cell tumors considered in the differential diagnosis of RMS. Formalin-fixed, paraffin-embedded archival tissue from 32 RMS, 107 non-RMS, and 11 benign skeletal muscle samples was stained for myogenin and MyoD1 with standard immunohistochemical techniques. Nuclear positivity was scored on a three-tiered scale. All RMSs expressed myogenin. Alveolar RMS (ARMS) showed strong nuclear staining, especially in tumor cells lining fibrous septae and perivascular regions. In cases with a subtle alveolar architecture on routinely stained sections, myogenin highlighted and enhanced visualization of the alveolar morphologic pattern. Embryonal RMSs (ERMSs) were more variable in myogenin staining pattern and intensity. No cases of nodular fasciitis, malignant fibrous histiocytoma, malignant peripheral nerve sheath tumor, inflammatory myofibroblastic tumor, myofibrosarcoma, leiomyoma, leiomyosarcoma, or alveolar soft part sarcoma stained for myogenin. Focal nuclear reactivity was seen in desmoid (2 of 10), infantile myofibromatosis (2 of 10), synovial sarcoma (1 of 10), and infantile fibrosarcoma (2 of 10). Non-neoplastic skeletal muscle fiber nuclei stained positively for myogenin in both tumor-associated samples (25 of 40) and benign skeletal muscle samples (5 of 11). Although all RMSs were immunoreactive for MyoD1, cytoplasmic and nonspecific background staining and reactivity of nonmyoid tissues hindered its practical utility in paraffin-embedded samples in this study. Although myogenin is a highly sensitive and specific marker for RMS, it is rarely seen in other spindle cell soft tissue tumors. As previously reported, ARMS stained more strongly than ERMS. In contrast to previous studies, rare non-RMS (7 of 107) displayed focal nuclear reactivity, and entrapped atrophic or regenerative skeletal muscle fibers also stained positively. Although these are potential pitfalls in the interpretation of myogenin, careful attention to morphology and other features, to the relative paucity of myogenin-positive nuclei in non-RMS. and to the presence of entrapped muscle fibers should prevent incorrect interpretation. Because the extent of myogenin expression in RMS is much greater than in non-RMS, it is a very useful marker when interpreted in the context of other clinicopathologic data.

Biomarkers, Tumor↗
PubMed1984

[Clinico-morphological analysis of bone fibrosarcomas (a retrospective study)].

The data on 35 cases of bone fibrosarcoma treated at the Center clinic in 1955-1982 are presented. A retrospective morphological investigation left diagnosis unchanged in 17 cases (48.6%). In 9 cases diagnosis was changed to fibrous histiocytoma of the bone, in 2--parostal sarcoma and in one case--"dedifferentiated" chondrosarcoma. In 6 cases, diagnosis could not be improved and neoplasms were identified as poly-morphocellular sarcoma. Clinically, a more favorable course and prognosis are distinguishing features of fibrosarcoma as compared with osteogenic sarcoma and malignant fibrous histiocytoma.

Adolescent↗
PubMed2001

Congenital-infantile fibrosarcoma. A clinicopathologic study of 10 cases and molecular detection of the ETV6-NTRK3 fusion transcripts using paraffin-embedded tissues.

Congenital-infantile fibrosarcoma (CIFS) is a relatively indolent sarcoma that should be distinguished from more aggressive spindle cell sarcomas of childhood. CIFSs have been found to have a novel recurrent reciprocal translocation t(12;15)(p13;q25) resulting in the gene fusion ETV6-NTRK3 (ETS variant gene 6; neurotrophic tyrosine kinase receptor type 3). We studied immunohistochemical expression of NTRK3, and conducted a reverse transcription-polymerase chain reaction (RT-PCR) assay to detect the ETV6-NTRK3 fusion transcripts using archival formalin-fixed paraffin-embedded tissues from 10 CIFSs. Thirty-eight other spindle cell tumors were included as controls. The ETV6-NTRK3 fusion transcripts were identified in 7 (70%) of 10 CIFSs. Nucleotide sequence analysis showed that the fusion occurred between ETV6 exon 5 and NTRK3 exon 13. The 38 control tumors were negative for the fusion transcript. Immunohistochemically, CIFSs consistently expressed NTRK3. But the expression of NTRK3 also was observed in 22 of 38 control tumors. These results show the diagnostic usefulness of RT-PCR methods to detect ETV6-NTRK3 fusion transcripts in archival formalin-fixed paraffin-embedded tissue and the important role of NTRK3 in the development of CIFS, despite its being a protein of little importance in differential diagnosis.

Child↗
PubMed2004

Oral etoposide for recurrent/progressive sarcomas of childhood.

BACKGROUND: Etoposide (VP-16) is a topoisomerase II inhibitor that is effective in a broad spectrum of pediatric and adult malignancies. Chronic, low-dose, oral VP-16 has also been shown to be active in some recurrent malignancies mostly in adults. The aim of this prospective, single institution study is to assess the efficacy and toxicity of oral VP-16 in children with progressive or recurrent (P/R) sarcomas. PROCEDURE: Twenty-one children (10 girls and 11 boys) with R/P sarcomas and a median age of 11 years (range 3-16 years) were enrolled in this study. The diagnosis was Ewing sarcoma family tumor (ESFT) in seven, osteosarcoma in eight, rhabdomyosarcoma in four, clear cell sarcoma of soft tissue in one, fibrosarcoma in one patient. Oral VP-16 was administered at a dose of 50 mg/m(2)/daily for 20 days. The next course was initiated after a 10 day rest. Response to oral VP-16 was assessed after two courses. RESULTS: There was an objective response (one complete response [CR], two partial responses [PR]) in three patients (14%) by two courses of oral VP-16 alone. One of these patients with PR achieved CR by the use of radiotherapy (RT) and further oral VP-16. Two more patients (9.5%) achieved CR by RT and oral VP-16. Eight (38%) patients had disease stabilization for 2-15 months. Two patients (9.5%) are long-term survivors. They are alive with no evidence of disease (NED) 79 and 94 months from time of relapse/progressive disease (PD). A patient developed acute myeloid leukemia and died. There was no major acute toxicity related to oral VP-16 in a total of 126 courses. CONCLUSIONS: Oral VP-16 therapy is simple, relatively nontoxic, and does not necessitate hospitalization. The cure rate is small. Given the risk of second malignancy, especially in children with previous exposure to topoisomerase II inhibitors and alkylating agents, this regimen may be used as a palliative treatment or in patients with poor prognosis.

Administration, Oral↗
PubMed2002

Gains of 12q are the most frequent genomic imbalances in adult fibrosarcoma and are correlated with a poor outcome.

Comparative genomic hybridization was used to analyze 41 adult fibrosarcomas from 34 patients. Thirty-one patients showed in their tumors DNA sequence copy number changes (mean 11, range 3-25). The minimal common regions for the most frequent gains were narrowed down to 12q21 (18 cases); 12q14-q15 and 14q22 (16 cases each); 4q22, 7q31, and 14q23-q24 (15 cases each); and 4q21, 4q23-q24, 8q22, and 12q22 (14 cases each). Twenty-five high-level amplifications were observed in 12 samples. 12q21 and 18p were affected three times each; and 1p21, 4q31.3, 7p21, 12q14-q15, Xp22.1-p22.2, and Xq22-q23 two times each. Losses were less frequent than gains. Early stages of adult fibrosarcomas were characterized by frequent gains of chromosomes 2, 4q, and 14q, whereas gains of chromosomes 7 and 8q were associated with progression. Gains of 12q were frequent in all of the developmental steps of this soft-tissue sarcoma. By investigation of several tumors of the same patient, a number of corresponding changes were always detected. Adult fibrosarcomas from patients who died during the observation time showed statistically significant more frequent gains of 8q, 12q, 13q, and 15q compared to the fibrosarcomas of patients who are alive. Gains and high-level amplifications of 12q14-q22, which were the most frequent genomic imbalances, partly reflected an MDM2 amplification, indicating the importance of this region in the tumorigenesis of sarcomas. In adult fibrosarcomas, a gain of 12q22 correlated significantly (P = 0.028) with a poor overall survival rate.

Abdominal Neoplasms↗
PubMed1989

Expression of c-sis and other cellular proto-oncogenes in human sarcoma cell lines and biopsies.

Six biopsies (4 of human fibrosarcomas, 1 of a B-cell lymphoma and 1 of a normal lymph node from a melanoma patient) and 6 cell lines (derived from 5 different human osteosarcomas and from 1 rhabdomyosarcoma), together with control cells, were examined for the expression of c-sis, c-fos and c-myc. The expression of c-sis/PDGF-B-related proteins was also examined in cultured cells (not in biopsies). In situ hybridization studies further showed that the occurrence and level of expression of c-sis mRNA and c-sis/PDGF-B-related proteins were significant in the tumor cells. Expression of c-fos and c-myc mRNA did not correlate with c-sis expression. Southern blot analysis of c-sis, c-fos and c-myc of 20 DNAs of cell lines derived from human sarcoma or biopsies showed an identical pattern for BamH1 and EcoR1 restriction fragments of c-sis (except for 1 fibrosarcoma biopsy), implicating no gene rearrangement as a cause of enhanced proto-oncogene expression. The nucleotide sequence of c-sis is highly homologous to that of the viral v-sis oncogene which is capable of transforming infected cells. We conclude that enhanced expression of c-sis in the sarcomas we have examined is involved in the initiation and/or maintenance of the cell transformed state.

Biopsy↗
PubMed1994

Myogenic regulatory protein expression in adult soft tissue sarcomas. A sensitive and specific marker of skeletal muscle differentiation.

Myogenic regulatory protein (MyoD1) is a DNA-binding nuclear protein that initiates myogenesis in mesenchymal stem cells. Its expression has proved a very sensitive marker of myogenic differentiation in malignant tumors of childhood. In this study, the reliability of MyoD1 expression as marker of skeletal muscle differentiation has been tested in 38 cases of adult-type sarcomas. Frozen sections were stained with the monoclonal antibody 5.8A (MAb 5.8A) developed against recombinant wild-type murine MyoD1. Routinely processed formalin-fixed sections from the same cases were reviewed and immunostained with a panel of antibodies commonly used to detect muscle differentiation: myoglobin, fast-myosin, desmin, muscle-specific actin, alpha-smooth muscle actin. Four cases positively stained with MAb 5.8A: three were high-grade spindle cell sarcomas, the fourth case was an alveolar soft-part sarcoma. Only tumors in which skeletal muscle histogenesis was inferred on the basis of histology and/or immunohistochemistry with conventional muscle markers stained positively for MAb 5.8A. All the other tumors tested, including leiomyosarcomas (11), liposarcomas, (10, including four dedifferentiated liposarcomas), fibrosarcomas (three), malignant fibrous histiocytomas (two), synovial sarcomas (two), and malignant peripheral nerve sheath tumors (two), were negative for MAb 5.8A. The high level of sensitivity and specificity of MyoD1 expression indicates the value of this marker in the diagnosis of soft tissue sarcomas.

Adolescent↗
PubMed1981

In vivo antigenic modification of tumor cells. I. Introduction of murine leukemia virus antigens on non-virus-producing murine sarcomas.

Murine oncovirus antigens represent excellent targets for immune recognition, and virus-associated tumors are generally susceptible to various immunotherapy protocols. Virus-negative tumors, however, are nonimmunogenic and refractory to immunologic control. Therefore, the feasibility of the introduction of antigens onto non-virus-expressing tumors in situ in inbred C57BL/6J mice by systemic administration of nononcogenic murine retroviruses was investigated. Two classes of murine fibrosarcomas were studied: a 3-methylcholanthrene-induced fibrosarcoma syngeneic to C57BL/6 mice (MCA-FS) and a Harvey murine sarcoma virus-transformed, nonproducer fibrosarcoma syngeneic to C57BL/6 mice (H-NP). Both were found to be devoid of infectious ecotropic murine leukemia virus (MuLV) or MuLV antigens. A single dose of Friend murine leukemia virus (F-MuLV) was used to superinfect MCA-FS- and H-NP-induced tumors in vivo and converted these tumors to a highly productive, virus-positive state. In vivo superinfected tumors were indistinguishable from their preinfected counterparts by competition radioimmunoassays for the virion's major envelope glycoprotein, gp71, and its group-specific antigen, p30, and by assays for infectious virus. Analysis of virus from tumor extracts proved that the antigenic specificity of the superinfected tumor was provided by F-MuLV administered systemically to the animals. Finally, an immunoperoxidase technique, applied to tumor cross sections, demonstrated the uniform appearance of viral antigens in the superinfected tumors.

Animals↗
PubMed1987

Fibrosarcoma mimicking breast fibromatosis.

Fewer than 1% of malignant breast tumors are sarcomas. Lack of correlation between the biologic behavior and histopathologic appearance of these tumors has been reported. A well-differentiated fibrosarcoma could be mistaken for breast fibromatosis, which may be a familial trait and may occur in Gardner syndrome. Forty-three cases of mammary fibromatosis have been reported. Most authors are concerned with misdiagnosis of breast fibromatosis as a malignant lesion leading to unnecessary mastectomy. However, the result can be disastrous when a well-differentiated fibrosarcoma is diagnosed as fibromatosis and the patient develops lung metastases.

Breast Neoplasms↗