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Biomedical subjects

E Bonmassar

Publications and source records attributed to E Bonmassar.

At least 163 records · Page 9Linked to original sources
PubMed1976

Suppression of allogeneic lymphomas in spleens of irradiated mice: importance of the D end of the H-2 complex.

Dispersed lymphoma cells were transplanted into heavily irradiated mice of a series of congenic resistant strains. Newly synthesized deoxyribonucleic acid was subsequently measured to estimate tumor cell proliferation in spleen and liver. Despite host irradiation, growth of lymphoma cells was suppressed 4 to 7 days after transplantation in the spleen of mice of certain allogeneic strains, but it was barely affected in the liver. The genetic differences resulting in "localized" resistance were mapped in the D region of the H-2 complex. Differences at other regions, including those most important for transplantation resistance in nonirradiated mice (K, I), were inconsequential for lymphoma growth in irradiated hosts. There was a striking resemblance with hemopoietic histoincompatibility, i.e., the rejection of foreign bone marrow grafts by irradiated mice, suggesting that the products of strong Hh gene(s) were expressed in the lymphoma cells.

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PubMed1976

A viral immunodepressive factor associated with experimental mouse tumors.

An immunodepressive factor (IDF) capable of inhibiting the rejection of allogeneic lymphomas in mice was detected in a number of transplantable mouse tumors. The allograft reactivity of the host was impaired for at least 10 months after IDF administration. No clinical evidence of bacterial or viral infection was detected in IDF-treated animals. Sera collected from mice at various intervals after injection of IDF showed a great increase in the IDF-titer. The IDF persisted in mouse sera for at least 3 months, whereas no IDF activity was found in sera of rats given injections of the factor. IDF was capable of replicating in vitro in mouse embryo cells, but not in rat embryo or HeLa cell cultures. IDF was inactivated in vitro by heat (65 degrees for 30 min), ultraviolet light or ether, but not by ethyl alcohol. These studies indicate that IDF is a virus capable of producing a long-lasting asymptomatic infection specifically interfering with the host's allograft reactivity. In several instances a close association between the lactic dehydrogenase virus and IDF was found. Nevertheless no conclusion was reached on the identity or nonidentity between the two viruses.

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PubMed1975

Increased immunogenicity of two lymphoma lines after drug treatment of athymic (nude) mice.

Highly immunogenic sublines of L1210 and LSTRA lymphomas were obtained from athymic (nude) mice treated with 4(5)-(3,3-dimethyl-1-triazeno)imidazole-5(4)carboxamide (DIC) in vivo. Conventional mice, compatible with the parent tumor, rejected the DIC-treated sublines and were relatively resistant to a subsequent challenge with the parent lines. The DIC-treated sublines were not rejected by athymic mice, which indicated that the transplantation resistance to these tumors in conventional mice was thymus-cell dependent. In addition, there was marginal or no increase of tumor-cell immunogenicity when the parent lines were passaged in nude mice without DIC treatment. This indicated that the DIC-dependent immunogenic changes in DIC-treated leukemic conventional mice could not be ascribed merely to protection by naturally occurring antigenic clones that resulted from DIC-induced immunodepression.

Animals↗
PubMed1975

Uptake of 5-iododeoxyuridine as a measure of tumor growth and tumor inhibition.

The DNA synthesis of tumor cells in spleen, lung and liver of mice bearing spontaneous or transplanted lymphomas or Lewis lung carcinoma was determined by measuring the uptake of 5-iododeoxyuridine labeled with iodine-125 (125IUdR). An in vitro uptake method was also developed to assess 125IUdR uptake of peripheral blood of leukemic animals. A direct relationship was found between isotope uptake values and the extent of neoplastic growth. The 125IUdR uptake method was found to be applicable to determination of inhibition of tumor growth in drug-treated animals and in pre-sensitized allogeneic hosts and to measurement of regression in non-sensitized allogeneic mice.

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PubMed1975

Immune inhibition of allogeneic lymphoma cells in the peritoneal cavity of mice.

Mice were sensitized with cells of normal spleen, transplantable syngeneic lymphomas, or allogeneic lymphomas differing for alloantigens specified by the major histocompatibility complex. From three to eleven days later, the allograft reactivity of these sensitized and appropriate control mice was evaluated in the peritoneal cavity by the disappearance of injected lymphoma cells or the inhibition of DNA synthesis. For the disappearance test, target cells were labeled with [125-I]-5-ido-2'-deoxyuridine before transfer. For the inhibition test, unlabeled target cells were transferred, but these cells were subsequently exposed to the DNA precursor [125-I]-5-iodo-2'-deoxyuridine. In both procedures, cells were recovered from the peritoneal cavity without killing the hosts to measure retained radioactivity. Both tests were immunogenetically specific in detecting secondary allograft reactions, but the disappearance test was less sensitive. By inhibition of DNA synthesis, it was possible to detect primary and secondary reactions, the latter three to eight days after sensitization. Alloantigens associated with the H-2K-Ir regions of Murine Linkage Group IX were more immunogenic than those associated with the Ss-H-2D-Tla regions in eliciting antilymphoma reactions, and female mice responded better than males. It was concluded that the peritoneal inhibition test is sensitive enough to monitor transplantation immunity in vivo and could be applied to animals bearing tumors in sites other than the peritoneum and undergoing chemotherapy.

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PubMed1975

Changes of the immunogenic properties of a radiation-induced mouse lymphoma following treatment with antitumor drugs.

Eight sublines of the radiation-induced lymphoma S-1033 of C57BL/10 (hereafter called B10) origin were established by exposing the cells in vivo to eight antineoplastic agents for a number of transplant generations. The parental and drug-treated sublines were tested for immunogenic properties, i.e., the ability to elicit allograft reactions in the host of origin and in congenic-resistant mice differing for the S-D or K-I-S regions of the H-2 complex. Lymphoma S-1033 and all drug-treated sublines except one were found to be essentially nonimmunogenic for B10 mice. The S-DIC subline, when exposed for 8 to 12 transplant generations to dimethyltriazenoimidazolecarboxamide, became immunogenic for syngeneic B10 mice, as judged from prolongation of survival time. Large i.v. inocula (10(7) cells) of S-1033 and of the drug-treated sublines, with the possible exception of the cyclophosphamide-treated and dimethyltriazenoimideazolecarboxamide-treated lymphomas, were more effectively rejected by K-I-S- than by S-D-incompatible mice. Dilution escape (i.e., tumor rejection after challenge with large inocula, and lethal tumor growth after injection of small inocula of lymphoma cells in allogeneic recipients) occurred in K-I-S-incompatible mice that were inoculated with S-1033 and three drug-treated (5-fluorouracil, cyclophosphamide, and pyrazocarboxamideamino) sublines. No dilution escape occurred with dimethyltriazenoimidazolecarboxamide or bischloroethylnitrosourea sublines. These data favor the hypothesis that various types of immunogenic changes of neoplastic cells may occur in tumor-bearing hosts following treatment with antineoplastic agents in vivo.

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PubMed1970

Immunological alteration of leukemic cells in vivo after treatment with an antitumor drug.

L1210 leukemia was transplanted serially in CDF(1) mice treated with 5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide (DIC, NSC 45388). After four different lines (C lines) had been treated for several generations, a marked increase in survival time of untreated mice was observed. In contrast, mice treated with DIC or immunosuppressed with cyclophosphamide succumbed earlier with generalized leukemia. Furthermore, a C line showed unusually high sensitivity to chemotherapeutic treatment with 1,3 bis(2-chloroethyl)-1-nitrosourea. The data suggest that C lines acquired strong antigenicity for CDF(1) and DBA/2 hosts. DIC treatment may have selected highly antigenic variants or induced somatic mutations resulting in the appearance of strong new transplantation antigen(s).

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