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At least 1,279 records · Page 71Linked to original sources
PubMed1985

Splenotoxicity associated with splenic sarcomas in rats fed high doses of D & C Red No. 9 or aniline hydrochloride.

A histopathologic review of F344 rat spleens from the National Toxicology Program-National Cancer Institute bioassays of barium salt of 5-chloro-2-(2-hydroxy-1-naphthalenyl)-azo-4-methylbenzenesulfonic acid [(D & C Red No. 9) CAS: 516-00-21] and aniline HCI (CAS: 142-04-1) was conducted to assess splenotoxic changes associated with splenic sarcomas induced by these aromatic amines. Four splenic changes--fatty metamorphosis (FM), splenic fibrosis (FIB), capsule hyperplasia (CH), and hemorrhage--were markedly increased in incidence and severity in males treated with high doses of either D & C Red No. 9 or aniline HCI. Females treated with high doses of either of these compounds showed similar but less severe changes. FIB and FM showed strong group correlations with tumor incidence (r greater than or equal to 0.87). All groups that demonstrated FM also demonstrated splenic sarcomas; groups without the FM lesions did not exhibit splenic tumors. The morphologic similarity of the FIB and CH lesions to the induced splenic sarcomas suggests that these lesions are preneoplastic. Moreover, the treatment-related splenic lesions appear to be precursors of the induced splenic sarcomas. Carcinogenicity studies with serial sacrifices at varying intervals will be required for experimental verification of these conclusions. A schema, based on the findings of the study, suggests a hypothetical pathway for the progression of the treatment-related splenic lesions from onset to tumor formation.

Aniline Compounds↗
PubMed1999

Effects of genistein on invasion and matrix metalloproteinase activities of HT1080 human fibrosarcoma cells.

Effects of genistein on invasion and matrix metalloproteinase activities were investigated in HT1080 human sarcoma cells. Invasion of HT1080 cells through reconstituted basement membrane was inhibited when the cells were treated with 100 micromol/L and 200 micromol/L genistein. At the same concentrations, genistein not only suppressed latent forms of matrix metalloproteinase-2 and -9 (MMP-2 and MMP-9) to convert into active forms, but also increase dramatically the tissue inhibitor of metalloproteinase (TIMP-1) mRNA contents and reverse the imbalance of MMPs and TIMPs. However, expressions of MMP-2 and MMP-9 were not significantly affected. Suppression of MMP activation and increase of TIMP-1 expression will decrease matrix degradation by MMPs, and consequently inhibit invasions of the cells. These results emphasized the existence of the imbalance between MMPs and TIMPs in tumor invasion and metastasis formation. The value of genistein as a drug for antiinvasion and anti-metastasis chemotherapy was suggested.

Antineoplastic Agents↗
PubMed1998

Inflammatory fibrosarcoma: update, reappraisal, and perspective on its place in the spectrum of inflammatory myofibroblastic tumors.

Inflammatory fibrosarcoma (commonly referred to as inflammatory myofibroblastic tumor) has become increasingly recognized as part of a spectrum of inflammatory myofibroblastic proliferations. It is a potentially locally aggressive myofibroblastic tumor that occurs predominantly in the mesentery of children and young adults. No reliable morphological parameters have been identified that predict prognosis. We evaluated the ultrastructural and immunophenotypic features of 16 cases of inflammatory fibrosarcoma and studied Ki67 (MIB1), PCNA, bcl-2, and p53 in an effort to identify prognostic markers. p53 was not detected immunohistochemically in any case. None of the markers were found to correlate with local recurrences, metastases, or tumor deaths. Low proliferative activity (Ki67 < 10%) was seen in all cases. A characteristic immunophenotype was reconfirmed in which lesional myofibroblasts stained for vimentin, alpha-smooth muscle actin, cytokeratins, and rarely desmin. Ultrastructural studies of seven cases confirmed the presence of a fibroblastic-myofibroblastic spectrum. Because inflammatory myofibroblastic tumor-inflammatory fibrosarcoma is associated with systemic symptoms, polymerase chain reaction studies for Epstein-Barr virus (EBV) and cytomegalovirus (CMV) were performed in 12 cases. Evaluable results in nine cases did not show evidence of either virus. The results of this study indicate that inflammatory fibrosarcoma has a low proliferative activity, which is in keeping with the impression that this is a low-grade sarcoma; that myofibroblasts can participate in true neoplasia; and that EBV and CMV do not play a role in the pathogenesis of inflammatory fibrosarcoma. The variable phenotype of the myofibroblast and its role in reactive and neoplastic processes are discussed. A perspective on the position of inflammatory fibrosarcoma in the spectrum of inflammatory myofibroblastic tumors is also given in light of the current study and the literature.

Adolescent↗
PubMed1998

A novel ETV6-NTRK3 gene fusion in congenital fibrosarcoma.

Congenital (or infantile) fibrosarcoma (CFS) is a malignant tumour of fibroblasts that occurs in patients aged two years or younger. CFS is unique among human sarcomas in that it has an excellent prognosis and very low metastatic rate. CFS is histologically identical to adult-type fibrosarcoma (ATFS); however, ATFS is an aggressive malignancy of adults and older children that has a poor prognosis. We report a novel recurrent t(12;15)(p13;q25) rearrangement in CFS that may underlie the distinctive biological properties of this tumour. By cloning the chromosome breakpoints, we show that the rearrangement fuses the ETV6 (also known as TEL) gene from 12p13 with the 15q25 NTRK3 neurotrophin-3 receptor gene (also known as TRKC). Analysis of mRNA revealed the expression of ETV6-NTRK3 chimaeric transcripts in all three CFS tumours analysed. These were not detected in ATFS or infantile fibromatosis (IFB), a histologically similar but benign fibroblastic proliferation occurring in the same age-group as CFS. ETV6-NTRK3 fusion transcripts encode the helix-loop-helix (HLH) protein dimerization domain of ETV6 fused to the protein tyrosine kinase (PTK) domain of NTRK3. Our studies indicate that a chimaeric PTK is expressed in CFS and this may contribute to oncogenesis by dysregulation of NTRK3 signal transduction pathways. Moreover, ETV6-NTRK3 gene fusions provide a potential diagnostic marker for CFS.

Adult↗