Allogeneic Inhibition of Transplanted Tumor Cells*

Author(s):  
K. E. Hellstr�m ◽  
I. Hellstr�m
2009 ◽  
Vol 106 (33) ◽  
pp. 13832-13837 ◽  
Author(s):  
S. Hasegawa ◽  
K. Maruyama ◽  
H. Takenaka ◽  
T. Furukawa ◽  
T. Saga

1967 ◽  
Vol 13 (11) ◽  
pp. 1433-1444 ◽  
Author(s):  
R. Dubreuil ◽  
E. Di Franco ◽  
V. Pavilanis ◽  
P. Marois

The induction and the growth of viral SV 40 tumors in hamsters can be influenced by treating the animals with the oncogenic virus itself. The virus can be used to vaccinate against the transplanted tumor cells; it can also be used as a treatment to prevent the development of the tumor after its induction in the newborn by the virus or in the adult by the implantation of tumor cells.The present study reports that the administration of SV 40 virus to adult hamsters immediately following the excision of their transplanted SV 40 tumor brings a reduction in the frequency of recurrences appearing after the operation. It was also observed that among the animals that did not present recurrences after 7 to 10 months, those that were treated with the virus at the time of the surgical intervention, were still more resistant to the reimplantation of homologous cancer cells.These observations are interpreted as another indication that the evolution of a tumor can be modified in a favorable way by immunological means, in this instance, by a treatment with the oncogenic virus itself.


1963 ◽  
Vol 3 (8) ◽  
pp. 370-376 ◽  
Author(s):  
George F. Gitlitz ◽  
Arthur G. Ship ◽  
J. Leslie Glick ◽  
Arthur H. Glick

2021 ◽  
Vol 15 (1) ◽  
pp. 49-60
Author(s):  
M. D. Lootsik ◽  
◽  
R. S. Stoika ◽  

Introduction. An acquired resistance to experimental tumors was detected in animals that recovered from a primary transplanted tumor due to treatment or spontaneously, and demonstrated intolerance to a renewal tumor inoculation. This phenomenon is much less frequently observed, although it is of great scientific interest and medical significance. Here, we have addressed the expression of the resistance phenomenon in a model tumor in mice – Nemeth–Kelner lymphoma (NK/Ly). The aim of our study was to elaborate a reproducible method for induction of resistance to transplantation of lymphoma NK/Ly in mice and to investigate the mechanisms of its development. Methods and Results. Three schemes for induction of resistance were tested. The first one included treatment of tumor-bearing mice with vinblastine and, thereafter, reconvalescent animals were checked for the development of resistance expressed as a complete suppression of tumor growth after re-inoculation of tumor cells. Mice were inoculated intraperitoneally with NK/Ly ascitic cells and then subjected to 2–4 intraperitoneal injections of vinblastine at a dose of 1mg/g of body weight. The recovered mice were re-inoculated with tumor cells and the absence of tumor growth was considered as resistance development. The disadvantage of this approach is that less than 5% of mice achieve a long lasting recovery due to the treatment. The second scheme included the immunization of mice with intraperitoneal injection of the minimal number of viable tumor cells that do not cause tumor growth, but initiate the immune response. However, this approach was not effective, since there was no reliable number of cells correspon­ding to these demands. The minimal number of 15×103 injected cells per mouse caused a retarded but still progressive tumor growth. In the third scheme, the immunization of mice was conducted by the intraperitoneal injections of NK/Ly cells permeabilized with saponin. It should be noted that treatment with saponin leads to cell death with a minimal damage to cell morphology. The scheme of immunization with permeabilized NK/Ly cells appeared to be simple and effective. It provided a reproducible resistance to transplanted tumor and might be used as a model in studies of the mechanisms of this phenomenon. Cytological investigation of tumor and immunocompetent cells in ascites of control and of tumor-resistant mice was conducted. As revealed, the number of lymphocytes in ascites of tumor-resistant mice was about 4 times higher than such amount in the control (non-resistant) mice. A destruction of tumor cells by the adherent mono-nuclears was observed. Conclusions. The method of induction of resistance to transplantation of experimental tumor NK/Ly by immunization of mice with tumor cells permeabilized with saponin is described. The intraperitoneal inoculation of tumor cells to the tumor-resistant mice caused the marked increase of the mononuclear leukocytes population in the peritoneal fluid, which showed a harmful effect upon tumor cells. Thus, the induction of resistance to transplantation of NK/Ly lymphoma in mice might be provided mainly via the mechanisms of cell immunity, in particular, by the appearance of cytotoxic lymphocytes specific to distinct tumor cells.


2019 ◽  
Vol 68 (4) ◽  
pp. 569-576 ◽  
Author(s):  
Daisaku Takai ◽  
Akiko Abe ◽  
Heita Miura ◽  
Satoshi Tanaka ◽  
Jun-ichiro Komura

Author(s):  
C. N. Sun ◽  
C. Araoz ◽  
H. J. White

The ultrastructure of a cerebral primitive neuroectodermal tumor has been reported previously. In the present case, we will present some unusual previously unreported membranous structures and alterations in the cytoplasm and nucleus of the tumor cells.Specimens were cut into small pieces about 1 mm3 and immediately fixed in 4% glutaraldehyde in phosphate buffer for two hours, then post-fixed in 1% buffered osmium tetroxide for one hour. After dehydration, tissues were embedded in Epon 812. Thin sections were stained with uranyl acetate and lead citrate.In the cytoplasm of the tumor cells, we found paired cisternae (Fig. 1) and annulate lamellae (Fig. 2) noting that the annulate lamellae were sometimes associated with the outer nuclear envelope (Fig. 3). These membranous structures have been reported in other tumor cells. In our case, mitochondrial to nuclear envelope fusions were often noted (Fig. 4). Although this phenomenon was reported in an oncocytoma, their frequency in the present study is quite striking.


Sign in / Sign up

Export Citation Format

Share Document