Primary epithelioid sarcoma of the scalp.

This article retrospectively reviewed a case of epithelioid sarcoma of the scalp; a treatment plan for this type of neoplasm has not been well defined in the literature because of the rarity of sarcomas in general and sarcomas located in the head and neck in particular. No comparative results can be drawn when dealing with such lesion in the scalp. Early recognition with an aggressive approach to confirm the existence of an epithelioid sarcoma is mandatory; a high index of diagnostic awareness is needed to recognize this uncommon tumor. Early diagnosis can only be auspicious. Early wide surgical resection is imperative to ensure better control of imperceptible tumor extension, and well-planned diagnostic and therapeutic intervention, rather than isolated management and referral for adjunctive treatment, is important.     

Polymorphism of avian sarcoma virus src proteins.

The src gene products of seven different avian sarcoma viruses were compared. In vitro translation of virion RNA yielded products identified unambiguously as p60src in the case of two stocks of the Schmidt-Ruppin strain, three stocks of the Prague strain, the Bryan strain, and the Bratislava 77 strain of avian sarcoma virus. Differences in the electrophoretic mobility of these seven p60src proteins in sodium dodecyl sulfate-polyacrylamide gels, corresponding to variation in the apparent molecular weights ranging from 56,000 to 60,500, were observed. Antigenic variability was also found; only three of the seven viruses tested encoded a p60src, which was precipitated by antisera derived from rabbits bearing tumors induced by the Schmidt-Ruppin strain of Rous sarcoma virus. Examination of the methionine-containing tryptic peptides of the seven ;60src proteins by two-dimensional mapping revealed four common peptides but marked variability in the five to eight other peptides in each protein. Clear differences in the peptide maps of p60src were observed, both between different strains of virus and within strains. In the three cases examined, p60src synthesized in transformed cells was found to be essentially identical to that synthesized in vitro. We conclude that there is significant polymorphism in the p60src proteins of the avian sarcoma viruses.     

Digital cell image analysis of Ewing's sarcoma.

We analyzed the lesional tissue in Ewing's sarcoma by means of a cell image processor computing 15 nuclear parameters in order to quantify the morphologic variability of the tumor cell nuclei. To this end we combined 32 cases (350-400 Feulgen-stained nuclei analyzed per case) in a data file, which was then subjected to principal component and canonical analyses. We found considerable heterogeneity within the cell nucleus population of Ewing's sarcomas. Indeed, after the arbitrary subdivision of the file into two cell classifiers (CC1 and CC2 cell types) on the basis of the first canonical function, the 32 Ewing's sarcomas showed a great deal of variability in the proportion of CC1 and CC2 cell nucleus types. The nuclei of the CC1 type had a more finely textured chromatin when compared to the CC2 type, the nuclei of which exhibited a more granular chromatin pattern. Additionally, these 32 Ewing's sarcomas were characterized by three distinct DNA histogram types. Eight tumors displayed a diploid nonproliferating DNA histogram pattern (type A), 11 a diploid proliferating (type B) and 13 an aneuploid (type C) DNA histogram profile. We found a highly significant relationship between these DNA histogram types and the CC1:CC2 cell type percentage ratio. The eight Ewing's sarcomas with a type A DNA histogram contained a significantly higher proportion of CC1 cell type nuclei as compared to the 13 tumors with a type C DNA histogram, which contained a great proportion of CC2 cell type nuclei.     

Envelope assembly mutant of rous sarcoma virus.

The properties of a novel nonconditional envelope mutant of Rous sarcoma virus, rdPN3/2-SR-D, defective in the assembly of viral glycoproteins into mature virions, are described.     

Sensitivity of Ewing's sarcoma to TRAIL-induced apoptosis.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is able to kill transformed cells. We have studied the expression and functionality of the TRAIL apoptotic pathway in Ewing's sarcoma. We demonstrate that tumors from patients with Ewing's sarcoma express receptors TRAIL-R1 and -R2. Using a panel of nine Ewing's sarcoma cell lines TRAIL could induce apoptosis in seven cell lines. Preincubation with interferon-gamma rendered the two resistant cell lines sensitive. TRAIL was the most potent inducer of apoptosis when compared to Fas ligand or TNF. TRAIL-mediated apoptosis could be inhibited by various caspase-inhibitors. No difference in the surface expression of TRAIL-receptors was observed between sensitive and resistant cell lines. Also, all cell lines had similar levels of expression of Flice-like inhibitory protein (FLIP) on immunoblot. However, the two resistant cell lines had only very low level expression of caspase 8 on RNA and protein level. In summary, we show that Ewing's sarcoma expresses receptors for TRAIL, and that cells are exquisitely sensitive to TRAIL-mediated apoptosis. These results may warrant clinical trials with TRAIL in Ewing's sarcoma once the safety of TRAIL for humans has been established.     

Effect of aphidicolin on avian sarcoma virus replication.

We studied the effect of aphidicolin, an inhibitor of eucaryotic DNA polymerase alpha, on viral DNA replication and integration during the first 24 h after infection of quail embryo fibroblasts with avian sarcoma virus. In drug-treated cells, the synthesis of unintegrated linear viral DNA species was not impaired; however, the subsequent accumulation of circular viral DNA species and integrated proviral DNA was reversibly inhibited. After removal of the drug, circular viral DNA species were derived from preexisting linear viral DNA species, instead of being derived by de novo synthesis.     

Plaque assay of avian sarcoma viruses using casein.

The caseinolytic activity of several strains of Rous sarcoma virus (RSV), conditional and nonconditional mutants of RSV, and nontransforming avian leukosis viruses was investigated. Only those viruses capable of transforming chick fibroblasts in vitro induced lysis of casein incorporated into an agar overlay. Lysis produced distinct clear areas in the turbid casein-agar gel which allowed a quantitative "plaque" assay of cell transformation. Casein plaque formation could not be separated from morphological conversion in cultures infected by wild-type RSV strains. In plates infected by mutants temperature sensitive for transformation, the caseinolytic activity appeared to be affected by temperature to a lesser extent than morphological conversion.     

Structure-function relationship of Rous sarcoma virus leader RNA.

Cells infected by RSV synthesize viral 35S RNA as well as subgenomic 28S and 22S RNAs coding for the Env and Src genes respectively. In addition, at least the 5' 101 nucleotides of the leader are also conserved and we have shown previously that this sequence contains a strong ribosome binding site (J.-L. Darlix et al., J. Virol. 29, 597). We now report the RNA sequence of Rous Sarcoma virus (RSV) leader RNA and propose a folding of this 5' untranslated region which brings the Cap, the initiation codon for Gag and the strong ribosome binding site close to each other. We also show that ribosomes protect a sequence just upstream from initiator Aug of Gag in vitro, and believed to interact with part of the strong ribosome binding site according to the folding proposed for the leader RNA.     

Tumor-associated antigens of rat moloney sarcoma cells. II. Cytosol antigens.

Rat Moloney sarcoma cells (MST) were pulsed with 35S-L-methionine for 10 and 60 min and lysed by vortexing in 0.5% deoxycholate, 0.5% NP40, 0.02 M Tris, 0.05 M NaCl, pH 7.5, for 30 sec. The lysate was centrifuged at 16,300 X G for 10 min and the supernatant was co-precipitated with Ig fractions of normal BN serum, normal Lewis serum, BN antiserum to Moloney sarcoma cells (BNaMST), BN antiserum to tumor-associated antigens (BNaTAA), BN antiserum to murine leukemia virus (BNaMuLV), BN antiserum to p30 (BNap30), BN antiserum to gp70 (BNagp70), Lewis antiserum to BN (LeaBN), and BN antiserum to BC5 tumor (BNaBC5). With BNaTAA and BNaMST, a cytoplasmic TAA with m.w. 85,000 was detected. In addition, BNaTAA detected three other species of cytoplasmic TAA with m.w. 220,000, 170,000 and 39,000.     

Rous sarcoma virus glycoproteins contain hybrid-type oligosaccharides.

Examination of [3H]mannose-labeled glycopeptides from Prague C Rous sarcoma virus gp85 with gel filtration and sequential glycosidase digestions demonstrated the presence of hybrid-type asparaginyl-oligosaccharides. The major hybrid species had an oligomannosyl core (Man5GlcNAc2-ASN) characteristic of neutral structures, plus "branch" sugars (NeuNAc-Gal-GlcNAc-) characteristic of complex, acidic structures.