[Lymphocyte-macrophage interaction in the rejection reaction against isologous and homologous ascites tumors (author's transl)].
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Animals↗
Biomedical subjects
A Nista
Publications and source records attributed to A Nista.
IgM participation in tumor rejection by immunized mice.
IgG and IgM participation in tumor rejection was studied in DBA/2 mice immunized against L1210 leukemia and in Swiss mice immunized against Ehrlich adenocarcinoma. In both the systems, IgM globulins seem to be implicated and are present on the cell surface of macrophages, lymphocytes and cancer cells, while IgG globulins are present only on some lymphocytes. IgM are also present in the peritoneal washing fluids (obtained 24 h of the control group. In the former group, protein content is about three times higher than that in the control group, while the relative amount of heavy proteins (18 S) and light proteins (7 S) is quite similar. These observations are discussed, as is the possibility that some complement components as C3 may participate in the reaction.
Animals↗
Effects of VM-26 and lonidamine on a B16 melanoma cell line.
The treatment of exponentially-growing B16 melanoma cells with teniposide causes a dose- and time-dependent decrease of cell survival. By means of the nucleoid technique, the formation of double strand breaks was demonstrated in the nuclei of the treated cells, indicating a possible involvement of topoisomerase II. DNA double strand breaks were rapidly but ineffectively repaired. Morphometric and densitometric analyses showed that teniposide treatment causes a considerable increase of nuclear area, nuclear DNA and cell size, associated with a lowering of the mitotic index to less than one hundredth of that of the controls. The cytocidal effect of VM-26 can be potentiated by the addition of a non-lethal dose of lonidamine, whose synergism is particularly evident at low teniposide concentrations.
Animals↗
beta 1-Integrin expression and function in human bladder cancer cells: modulation by TNF alpha.
Cytofluorimetric and biochemical analysis in two different grade human bladder cancer cell lines showed that G3 EJ cells exhibited higher levels of alpha5beta1 and alpha6beta1 heterodimers, and the G2 RT112 cell line higher levels of alpha2beta1. Alpha6/beta4 receptor was detected only in RT112 cells. Adhesion assays with extracellular matrix proteins indicated that both cells bound to fibronectin, laminin and collagen 1, the adhesive properties being related to the integrin profile. Inhibition tests revealed that alpha5beta1 mediated adhesion to fibronectin, alpha3beta1 and alpha6beta1 to laminin, and that alpha2beta1 was the main mediator of adhesion to collagen I in both cell lines. In EJ but not in RT112 cells, tumor necrosis factor-alpha induced the upregulation of alpha2, which mediated increased adhesion to collagen I. The different effects of TNFalpha on the two cell lines were not attributable to differences in tumor necrosis factor responsiveness, as both cells expressed comparable levels of tumor necrosis factor receptor-1 and the tumor necrosis factor-inducible intercellular adhesion molecule-1.
Carcinoma, Transitional Cell↗