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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expression of fine and intermediate cytofilaments in 10 cutaneous and seven subcutaneous leiomyosarcomas was studied immunohistochemically. All the tumors contained tumor cells which showed a positive immunoreactivity for desmin in formaldehyde-fixed and paraffin-embedded sections, but none of the seven anti-desmin antibodies used alone produced a distinct positive staining in all the tumors. A lack of correspondence in terms of immunoreactivity between tumor cells and the supposed muscle of origin was observed, especially in the subcutaneous leiomyosarcomas. In all cases, antibodies to muscle-specific and smooth muscle-specific actin were found to produce a positive staining in both the tumors and the supposed muscle of origin. Vimentin was detected in 8/10 cutaneous and 4/7 subcutaneous leiomyosarcomas, while the supposed muscle of origin was positive in 3/10 and 7/7 cases, respectively. Four of the cutaneous and three of the subcutaneous leiomyosarcomas contained tumor cells which stained positively for cytokeratins, while the supposed muscle of origin showed no positivity. It thus appears that a phenotypic shift in terms of vimentin and cytokeratin expression occurs in the tumor cells of cutaneous and subcutaneous leiomyosarcomas compared with the supposed muscle of origin. It is recommended that more than one monoclonal anti-desmin antibody is used to characterize these tumor entities. It is also concluded that the immunoreactivity for muscle-specific actins in superficial leiomyosarcomas is more constant, although less specific, than that of desmin and that the demonstration of the simultaneous expression of muscle-specific actins and desmin is helpful.
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PMID:Intermediate and fine cytofilaments in cutaneous and subcutaneous leiomyosarcomas. 171 44

Making the morphologic distinction between chronic pancreatitis and pancreatic adenocarcinoma is a diagnostic challenge in small biopsy specimens and fine-needle aspiration samples. It has been suggested that immunohistochemical evaluation for the tumor-associated glycoprotein-72 antigen recognized by the monoclonal antibody B72.3 may be helpful in this setting. Formalin-fixed, routinely processed, paraffin-embedded tissue from 29 known cases of chronic pancreatitis and 31 cases of pancreatic adenocarcinoma were evaluated for reactivity with monoclonal antibody B72.3 using a standard avidin-biotin complex technique. Positive staining was seen in 26 of 31 adenocarcinomas (84%) and in 6 of 29 cases (21%) of chronic pancreatitis. Although monoclonal antibody B72.3 is more commonly reactive with pancreatic adenocarcinoma than with chronic pancreatitis, too many cases of chronic pancreatitis are reactive with this antibody for it to be useful as a diagnostic adjunct.
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PMID:Lack of specificity of monoclonal antibody B72.3 in distinguishing chronic pancreatitis from pancreatic adenocarcinoma. 172 Sep 18

The development of the hybridoma technology allows the identification of tumor associated antigens with monoclonal antibodies (mAbs). Employing this technology mAb Due ABC 3 was obtained by immunization of a BALB/c mouse with bladder tumor cell line SW 1710 and subsequent cell fusion of spleen cells with P3. X63.Ag8.653 mouse myeloma cells. MAb Due ABC 3, an IgM antibody, was found to recognize an antigen present in the membrane of tumor cells in 25 out of 28 (89%) transitional cell carcinoma specimens but rarely (three out of 25 specimens, 12%) on normal urothelial cells. Cross reactions were seen with proximal tubular epithelium of the kidney and seven out of 12 renal cell carcinomas examined. Furthermore, the antigen was expressed by granulocytes, some gastrointestinal epithelia, ovarian and breast carcinoma. The antigen recognized by mAb Due ABC 3 was stable to fixation with formaldehyde and paraffin emmbedding, different proteases, alkaline treatment and heat exposure up to 70C. Antigenicity was abandoned by incubation with periodate but not with neuraminidase treatment. The antigen could be extracted with chloroform/methanol suggesting the involvement of a glycolipid. Immuno-thin layer chromatography revealed a single lipid band reacting with mAb Due ABC 3 but not with anti-CD15, directed against the Lewis X antigen. Although not tumor-specific, mAbs directed against differentiation antigens may be of value for the investigation of cell transformations as well as for diagnostic use.
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PMID:Monoclonal antibody Due ABC 3 directed against transitional cell carcinoma. I. Production, specificity analysis, and preliminary characterization of the antigen. 172 39

Short-term studies (9 days) in the rat have demonstrated that formaldehyde-induced nasal epithelial lesions are associated with increases in surface epithelial cell proliferation rates. The present studies were designed, in part, to investigate cell proliferation rates in the nasal epithelium of rats exposed to formaldehyde for a longer duration in order to determine if correlations exist between (1) the concentration-response in cell proliferation rate with the previously published formaldehyde bioassay tumor response; (2) sites of increased cell proliferation and the regions of the nasal passages that exhibit formaldehyde-induced cytotoxicity; and (3) sites of increased cell proliferation and the regions of the rat nasal passages previously determined to be most susceptible to neoplasia (i.e., the lateral meatus and nasal septum of the anterior nasal passages). Another important endpoint of this study was to provide data for a comparison of formaldehyde-induced responses in rats with previous findings in rhesus monkeys. Fischer-344 rats were exposed to 0, 0.7, 2, 6, 10, or 15 ppm formaldehyde for up to 6 weeks and pulse labeled with tritiated thymidine prior to each scheduled termination. Exposure to formaldehyde at 6 ppm or higher induced site-specific lesions in the nasal respiratory epithelium and was associated with increases in cell proliferation rate which remained statistically elevated throughout the 6 weeks. While a direct correlation between sites susceptible to formaldehyde-induced nasal cancer and increased cell proliferation was not evident, results from the present studies did demonstrate a clear correlation between sites of cellular injury and increases in cell proliferation and a concentration-dependent response which correlated with the previously published formaldehyde bioassay tumor response. Furthermore, this work demonstrated that formaldehyde-induced responses in rats exposed to 6 ppm were morphologically similar to those reported in the rhesus monkey; however, the distribution of lesions between the two species differed significantly.
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PMID:Regional increases in rat nasal epithelial cell proliferation following acute and subchronic inhalation of formaldehyde. 174 23

The influence of formaldehyde-killed Escherichia coli strain Nissle 1917 (SK 22) on macrophages of C57BL/6 mice was investigated in vitro. It has been shown that SK 22 activated macrophages derived from bone marrow produced Interleukin-6 with high efficiency. In addition, SK 22 stimulated macrophages to secrete tumor necrosis factor, as measured by a bioassay. Furthermore, macrophages were activated by SK 22 to produce a 3 fold amount of oxygen radicals compared to the spontaneous oxygen radical production. In contrast to this finding, the phagocytic capacity of these macrophages was only slightly increased. The specific lysis of P 815 tumor cells by peritoneal macrophages after coincubation with SK 22 was measured using tumor cells prelabelled with radioactive 51Cr. The results of the in vitro experiments presented clearly show that the E. coli preparation SK 22 is an efficient immunomodulator of the unspecific immune system.
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PMID:[Immunomodulating effect of killed, apathogenic Escherichia coli, strain Nissle 1917, on the macrophage system]. 179 94

Several tumor target cell lines, prototypically K562 cells, are resistant to lysis by recombinant tumor necrosis factor (TNF alpha) but are killed by monocytes expressing membrane-associated TNF, suggesting that membrane TNF could account for monocyte-mediated cytotoxicity. Formaldehyde-fixed monocytes or extracted monocyte membrane fragments are cytotoxic to K562 target cells. Treatment of monocytes with interferon-gamma (IFN-gamma) increases cytotoxicity by live and fixed cells or by extracted monocyte membranes. Both TNF and TNF receptors are detectable on monocyte membranes by FACS analysis, and the levels of each are modulated by treatment with IFN-gamma. Cytotoxicity can be inhibited by either anti-TNF or anti-TNF receptor antibodies. Incubation of effector cells with exogenous soluble TNF prior to fixation or membrane preparation increases their cytotoxicity. In contrast, incubation of the target cells with exogenous TNF neither increases nor decreases killing by effector cell membrane fragments or intact effector cells. The data suggest that the TNF receptors on the effector cell, but not on the target cell, play a crucial role in TNF-mediated cytotoxicity.
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PMID:The principal tumor necrosis factor receptor in monocyte cytotoxicity is on the effector cell, not on the target cell. 184 24

We compared macrophage binding and killing of F5b cells to the binding and killing of P815 mastocytoma cells and to several other nontransformed and transformed cell lines. Formalin fixation of elicited or activated macrophages did not affect binding of F5b or 3T3 cells but did abrogate binding of P815 cells. However, formalin fixation abrogated resident macrophage binding of F5b and 3T3 cells. Therefore, depending on the type of macrophage or target cell, formalin fixation may affect binding. Only the binding of P815 cells was dependent upon activation; macrophage binding of target cells F5b and 3T3 was not. Even though macrophages bound F5b and 3T3 cells, macrophages only mediated contact-dependent cytotoxicity against F5b cells. Macrophages did not kill 3T3 cells. Experiments also compared macrophage binding and killing of the uv-light-induced tumor cell lines 1422, 2237, and 2237a46. Only the cell line 2237a46 was susceptible to contact-dependent killing. Both 1422 and 2237 cells were resistant. In contrast, cell lines 2237a46 and 1422 were bound by activated macrophages while 2237 cells were bound poorly.
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PMID:Macrophage binding of cells resistant and sensitive to contact-dependent cytotoxicity. 189 60

Twenty tumors of the peripheral sympathetic nervous system were investigated using a spectrum of antibodies against vimentin, neurofilament triplet, S-100 protein, neuronal specific enolase (NSE), chromogranin, synaptophysin, and vasoactive intestinal polypeptide. There were two ganglioneuromas, seven stroma rich neuroblastomas (composite ganglioneuroblastomas), five undifferentiated and six differentiating stroma poor neuroblastomas (NB) included in the series. Formalin-fixed, paraffin embedded material was used. The results showed that reactivity of the antibodies was relatively high, except the reactivity against synaptophysin. The tumor cell population showed a heterogeneous positivity in all cases. Only some undifferentiated NB were positive with the employed antibodies, which reduces the diagnostic benefit in a group of NB in which diagnostic demands of the immunohistochemistry are most important. The best results in undifferentiated NB were obtained with polyclonal antibody against NSE. This antibody is, however, not specific. Positive results of the immunohistochemistry in this group of tumors should be evaluated with caution.
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PMID:[Tumors of the peripheral sympathetic nervous system in childhood. Immunohistochemical study]. 191 29

Many malignancies exhibit distinct patterns of metastasis that appear to be mediated by receptor/ligand-like interactions between tumor cells and organ-specific vascular endothelium. In order to study endothelial cell surface molecules involved in the binding of metastatic cells, we developed a perfusion method to isolate outside-out membrane vesicles from the lumenal surface of rat lung microvascular endothelium. Lungs were perfused in situ for 4 h at 37 degrees C with a solution of 100 mM formaldehyde, 2 mM dithiothreitol in phosphate-buffered saline to induce endothelial cell vesiculation. Radioiodinated rat lung endothelial cell membrane vesicles bound lung-metastatic tumor cells (B16F10, R323OAC-MET) in significantly higher numbers than their low or nonmetastatic counterparts (B16F0, R323OAC-LR). In contrast, leg endothelial membrane vesicle showed no binding preference for either cell line. Neuraminidase treatment of vesicles abolished specificity of adhesion of lung-derived vesicles to lung metastatic tumor cells. These results demonstrate that in situ perfusion is an appropriate technique to obtain pure endothelial cell membrane vesicles containing functionally active adhesion molecules. The preferential binding of lung-derived endothelial cell membrane vesicles by lung metastatic tumor cells is evidence of the importance of endothelial cell adhesion molecules in the formation of metastases.
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PMID:Endothelial cell membrane vesicles in the study of organ preference of metastasis. 198

Tumour cells possess the cell surface protease guanidinobenzoatase (GB) which can be located by the fluorescent probe 9-amino acridine (9-AA). Frozen sections and formaldehyde fixed sections of tumour tissue were used to demonstrate the interactions between GB, 9-AA and two protein inhibitors of GB. A cytoplasmic extract from the tumour tissue, and a purified inhibitor of plasminogen activator (PAI-1) were shown to be exchangeable components of the enzyme-inhibitor complex on the fixed tumour cell surfaces. The evidence suggests that GB is functionally very similar to plasminogen activator and that this enzyme can be regulated by protein inhibitors in vivo and also by changes in the redox potential at the cell surface.
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PMID:The inhibitor reacting with a tumour cell surface protease can be exchanged with plasminogen activator inhibitor (PAI-1). 203 70


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