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Biomedical subjects

C D Pasqualini

Publications and source records attributed to C D Pasqualini.

At least 73 records · Page 4Linked to original sources
PubMed1978

Antigenic differences between AKR lymphoma and thymus cells leading to detection of a tumor antigen associated with immunological enhancement.

In an experimental model conditioning for enhancement, an AKR lymphoma was made to grow in BALB/c mice, permitting the simultaneous comparison of tumor-bearing (progressor) and tumor-rejecting (regressor) animals. By immunofluorescence using as target AKR lymphoma and normal thymus cells, both acetone-fixed and unfixed, it was observed that the allogeneic progressor serum contained three antibodies, two of which could be asborbed by thymocytes while the other combined selectively with the acetone-fixed lymphoma target. This tumor-specific antibody could not be detected in regressor serum which, on the other hand, could be completely absorbed by thymocytes. The identification of this acetone-resistant tumor antigen led to the preparation of aceton-treated acellular lymphoma extracts: a precipitate was obtained which upon inoculation in BALB/c mice produced an antiserum that combined selectively with lymphoma targets. In vivo experiments showed that pretreatment with this antigen led to a significant increase in allogeneic tumor incidence, 76% as compared to 37% in the controls. It is concluded that in this allogeneic model, an acetone-resistant tumor-specific antigen and the corresponding antibody are involved in tumor enhancement.

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PubMed1978

Murine leukemia virus in chemically-induced sarcomas as detected by XC plaque formation.

To detect whether methylcholanthrene induced murine sarcomas contain endogenous murine leukemia viruses, direct XC syncytium assays were performed over short term tumor cultures. Out of 31 sarcomas, 13 (42%) induced more than 4 plaques per flask, while no such activity was found in 39 control spleen samples. It is postulated that the positive tests are related to an increase in the titer of endogenous B-tropic virus, probably as a result rather than as a cause of tumor induction by chemicals.

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PubMed1977

Enhanced growth of syngeneic Moloney sarcoma with decreased immunity in the regressors.

S.c. cellular transplants of MS tumours have a high incidence of rejection in adult BALB/c mice, which can then be used as syngeneic regressors. When these tumours were inoculated within a glass cylinder which had been implanted s.c. in BALB/c mice 2 days earlier, 51% of the animals died with progressively growing tumours, compared with 2% in animals which had received the same inoculum directly s.c. This experimental model demonstrates tumour enhancement in a syngeneic system, and duplicates what has been previously reported in two different allogeneic tumour-host combinations, where it was demonstrated that immunological enhancement was operating, since the addition of either progressor serum or soluble tumour antigen significantly increased tumour incidence. For the purpose of investigating whether the glass cylinder model could also modify the immune response of the host to a second tumour challenge, a leukaemia virus known to crossreact with MS was used. Regressors were challenged i.p. with a lethal dose of a leukaemia virus, PLLV. Regressors bearing a glass cylinder showed a 22% survival rate which was significantly lower than that of the s.c. inoculated regressors (71%). This decrease in cross-immunity suggests that the artificially constructed privileged site created by the glass cylinder, by conditioning for tumour enhancement, also decreases immunological memory.

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PubMed1977

Murine sarcoma virus pseudotypes used as immunogens against viral and chemical oncogenesis.

The purpose of this study was to develop an animal system of protective immunity against oncornaviruses and to test whether such immunization had an inhibitory effect upon chemical sarcomagenesis. Several murine sarcoma virus (MSV) pseudotypes were used as immunogens and tested against themselves, against other pseudotypes, against leukemogenesis by their helper viruses, and against sarcomagenesis by 3-methylcholanthrene. Five MSV pseudotypes were obtained by rescuing complete MSV from MSV-genome carrier, nonproducer hamster tumor cells, using five different leukemia viruses as helpers. The immunogenic properties of these pseudotypes could be specified on the basis of the following observations. 1) They all induced sarcomas in newborn mice and regressing sarcoma nodules in young adult mice. After regression, most mice remained free of neoplastic disease, but some developed sarcoma or leukemia relapses. 2) They had an individual host range pattern, usually determined by the helper virus, as tested by inoculation of a constant virus dose in BALB/c, C57BL/Ka, and Swiss mice. 3) They were all immunogenic, in the sense that the first virus inoculation prevented sarcoma induction by a second challenge, either viral or cellular. 4) They were cross-reactive in vivo, one pseudotype immunizing against another, in the combinations tested. 5) They were able to immunize against leukemogenesis induced by their helper viruses. This was shown by prevention of leukemic deaths by Rauscher and Friend viruses, by a slight prolongation of survival after challenge with the Precerutti-Law leukemia virus, and by inhibition of splenomegaly by Moloney leukemia virus. In a second stage of the study, we investigated whether immunization with any of the MSV psuedotypes had an inhibitory effect upon sarcomagenesis induced by near-threshold doses of 3-methylcholanthrene. The incidence of these sarcomas was essentially the same in virus-immunized and control mice. It was concluded that immunizing procedures able to prevent sarcomagenesis when the inducer is a virus did not have any consistent preventive effect when the inducer was a chemical.

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PubMed1976

An improved method for PHA-culturing mouse lymphocytes using Ficoll-Hypaque gradient.

A simple, reproducible method is described for in vitro culture of mouse lymphocytes purified by differential centrifugation through Ficoll-Hypaque gradient. Peripheral blood, spleen and thymus purified lymphocytes responded well to in vitro PHA stimulation as measured by blast transformation and tritiated thymidine incorporation; the lowest values were observed with thymus lymphocytes.

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PubMed1976

Phytohemagglutinin unresponsiveness of spleen cells of mice bearing an allogeneic lymphoma.

The in vitro response of spleen cells to phytohemagglutinin (PHA) was studied in BALB mice bearing an allogeneic AKR lymphoma (progressors). A significant decrease in blast transformation and DNA synthesis was observed in these animals as compared with those rejecting the tumor (regressors) or with unchallenged controls. It is postulated that either an alteration in PHA lymphocyte receptors or the presence of enhancing serum factors may be responsible for this decrease in PHA response.

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PubMed1976

Effect of a Rauscher leukemia virus vaccine upon chemical oncogenesis in the mouse.

The concept that type-C RNA viruses serve as determinants of chemically induced cancer would be supported if immunization against such viruses reduced the incidence of methylcholanthrene-induced sarcomas. A formalin vaccine was employed which was able to protect mice against the development of virus-induced Rauscher leukemia: 8/12 vaccinated mice survived versus 1/12 controls. When mice so immunized were challenged with near-threshold doses of chemical carcinogen, sarcoma incidence and death latency did not differ between vaccinated and control groups: within 10 months, a 320 mug dose of methylcholanthrene induced 100% sarcomas in both groups, while a 64 mug dose induced 62% and 65% tumors in vaccinated and control mice respectively. Thus, a relevant postulate of the oncogene hypothesis could not be supported by these studies. Formalin treatment neutralizes the oncogenic effect of mouse leukemia viruses yiwlding preparations that are immunogenic and can be successfully used as vaccines to protect against virus-induced leukemia (5). The finding of murine leukemia viruses in chemically induced tumors (1, 2) poses the question of whether these viruses are present in the tumors as passengers, or whether they are etiologically involved in the process of tumor induction. An approach to answering this question would be to challenge with chemical carcinogens mice which have been vaccinated with leukemia virus. If the virus were somehow involved in tumor induction, antiviral immunization might conceivably interfere with chemical carcinogenesis. Whitmire and Huebner (9) have reported that mice immunized with formalin-treated leukemia viruses, become resistant to sarcomagenesis by methylcholanthrene. Repetition of this experiment by Gericke and Chandra (6) gave non-significant differences between experimental and control groups. The present paper deals with the effect of immunization against Rauscher leukemia virus upon tumor induction by near-threshold doses of methylcholanthrene.

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PubMed1976

Murine leukemia induced by viral ultrafiltrates negative for XC plaque activity.

Leukemogenic activity has been encountered in 100 nm filtrates of a murine leukemia virus, PLLV-T2, associated with smaller than conventional C type particles. XC plaque assay of these filtrates gave negative results, revealing a lack of correlation between in vivo and in vitro activity. It is postulated that these filtrates contain viral subunits deficient for replication in BALB fibroblasts in vitro but able to transform lymphoid cells in vivo.

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PubMed1976

Conditions favoring immunological enhancement of a murine allogeneic lymphoma.

An in vivo model was used which permits the growth of AKR lymphoma allografts inoculated within a glass cylinder subcutaneously implanted in BALB mice. Pretreatment of the host with acellular tumor extracts or tumor cells enclosed within a diffusion chamber significantly increased tumor incidence. On the contrary, donor spleen extracts did not alter tumor incidence while viable spleen cells within a diffusion chamber even prevented tumor development. It can be concluded that in this model a condition of maximal tumor enhancement can be attained with soluble tumor antigen but not with normal spleen extracts.

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