Characterization of the presumptive sarcoma cells in primary MSV tumors

Becker, S; Haskill, Stephen

doi:10.1002/ijc.2910250417

Cited by 9 publications

(7 citation statements)

References 22 publications

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“…These results strongly suggest that reinfection of the second host is a very important mechanism in the successful "transplantation" of the lesion, and thus supports the notion of Simons (1970) (Becker & Haskill, 1980b) (Zinkernagel, 1979). Also, we wanted to re-examine our previous conclusion (Becker & Klein, 1980) that cytotoxic T cells are not generated in response to MSV in the A/Sn strain.…”

Section: Discussionsupporting

confidence: 69%

“…Although these macrophage cell fractions were inactive in the 16h 51Cr-release or microcytotoxicity experiments (Fig. 2) we have been able to show that these cells exert both cytostatic and cytolytic effects against the autologous "sarcoma" cells in 48h assays (Becker & Haskill, 1980b).…”

Section: Discussionmentioning

confidence: 72%

“…The supernatant was also tumorigenic, as 73% (11/15) Haskill, 1980b). To determine whether the cytotoxic tumour-infiltrating cells selectively kill virus+ cells, the immunoperoxidase-bridge method was used to stain the assay wells.…”

mentioning

confidence: 99%

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In vitro demonstration of in situ autologous tumour-cell cytotoxicity in MSV-induced tumours in A/SN mice

Becker¹,

Haskill²

1981

Br J Cancer

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Summary.-Moloney sarcoma-virus (MSV)-induced tumours in A/Sn mice have been dispersed with collagenase and DNase 8-15 days after virus inoculation, and both "sarcoma" and inflammatory cells separated by sedimentation velocity and adherence techniques. The isolated "sarcoma" cells had the morphological characteristics of atypical cells (i.e. cytoplasmic blebbing, vacuolization and prominent nucleoli) and were easily adapted to in vitro growth. As few as 2 x 103 of these cells inoculated i.m. produced new tumours within 8 days of injection in both syngeneic and allogeneic mice. Also, cell-free supernatant from "sarcoma"-cell cultures produced tumours, indicating that the successful transplantation of the "sarcoma" cells was probably due to production of infective virus. Cells cytotoxic in vitro against the ''sarcoma'' cells were present within both spleen and tumour of the tumour donors, but not in the spleens of normal mice. The cytotoxicity was specific against virusinfected cells, since in a mixture of virus-positive (gp 70) and virus-negative cells, positive cells were removed while negative cells were not affected, as measured by a visual cytotoxicity assay using immunostaining. Although T cells could be isolated from the MSV-induced tumours, these cells did not appear to mediate the cytotoxicity detected against the MSV "sarcoma" cells. These results suggest that early MSV infections might be sensitive to cytotoxic mechanisms distinct from those reported with established MLV-or MSV-induced tumour lines.

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Section: Discussionsupporting

confidence: 69%

Section: Discussionmentioning

confidence: 72%

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In vitro demonstration of in situ autologous tumour-cell cytotoxicity in MSV-induced tumours in A/SN mice

Becker¹,

Haskill²

1981

Br J Cancer

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“…The macrophages could not be purified from the "sarcoma" cells by adherence, since some of the "sarcoma" cells were highly adherent (Becker and Haskill, 1980a).…”

Section: Isolation and Purification Of Macrophages And Autochthonous mentioning

confidence: 98%

Non‐T‐cell‐mediated cytotoxicity in MSV tumor‐bearing mice. III. Macrophage‐mediated cytotoxicity against autochthonous MSV tumor‐isolated target cells

Becker

Haskill

1980

Intl Journal of Cancer

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Cytotoxic macrophages have been isolated from Moloney sarcoma virus (MSV) tumors induced in uncompromised, immunosuppressed and athymic nude mice. Macrophages from compromised mice were at least as active as those from uncompromised mice when tested against the autochthonous MSV target cells. Although both cytolytic and cytostatic activity could be demonstrated with all tumor-derived macrophages, cytostatic and cytolytic effects could be distinguished from each other only at high effector target-cell ratios. A variety of target cells were compared for sensitivity to the various tumor-associated macrophages. The autochthonous virus-infected MSV-target cells appeared to be more sensitive to the macrophage effects than fastgrowing, established cell lines. Normal embryo fibroblasts were only slightly affected. Peritoneal exudate cells from tumor-bearers were much less active than either the tumor-isolated macrophages or bone-marrow culture-derived macrophages. Both were more active than control peritoneal cells. Although no quantitative or qualitative differences in macrophage activity could be detected in mice with regressing lesions and immuno-compromised mice with progressing lesions, the ratio of macrophages to "sarcoma" cells was three to five times higher in regressing tumors.

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“…Mesenchymal cells, which are subsequently seen to proliferate in the local lesion and give rise to fibroblasts, are not typical of this process and may be characteristic of sarcomas. Yet the great majority of these tumors regress, and unlike other tumors they do not appear to develop by clonal proliferation, but may spread by reinfection of adjacent normal cells by virus, present at the local site in high concentration (Becker and Haskill, 1980). Accordingly regression could be thought to be due to elimination of the virus and cessation of virus production.…”

mentioning

confidence: 99%

Anti‐tumor immunity in b‐lymphocyte‐deprived mice. iii. immunity to primary moloney sarcoma virus‐induced tumors

Gordon

Holden

Segal

et al. 1982

Intl Journal of Cancer

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Tumor induction and immunity to tumors were studied following the injection of Moloney sarcoma virus (MSV) into mice whose B-lymphocyte functions had been suppressed by the chronic administration of anti-IgM antibodies. Two preparations of MSV were used; one which gives rise to tumors which uniformly regress in normal adult mice, and another which elicits progressively growing tumors in the majority of recipients. The tumor incidence, mean tumor size, and tempo of regression were not modified by treatment with anti-IgM. However, whereas tumors induced by the regressor virus were all rejected in 19 NRG-treated and 29 untreated recipients, continued growth was obtained in 2 of 23 B-lymphocyte-deprived mice. Furthermore, in 9 additional mice from this group, apparent rejection was followed by tumor recurrence at the site of the initial tumor. Continued growth was accompanied by widespread metastasis. These tumors were freely transplantable to normal syngeneic recipients. Metastasis and transplantability were also detected in 7 of 24 anti-IgM-treated mice given progressor virus, but were not seen in the control animals. Recurrence and metastasis was obtained despite the presence of high levels of specific cytotoxic T lymphocytes in the spleen. It is concluded that B lymphocytes or their products play an essential role in host protection against MSV-induced tumors.

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Characterization of the presumptive sarcoma cells in primary MSV tumors

Cited by 9 publications

References 22 publications

In vitro demonstration of in situ autologous tumour-cell cytotoxicity in MSV-induced tumours in A/SN mice

In vitro demonstration of in situ autologous tumour-cell cytotoxicity in MSV-induced tumours in A/SN mice

Non‐T‐cell‐mediated cytotoxicity in MSV tumor‐bearing mice. III. Macrophage‐mediated cytotoxicity against autochthonous MSV tumor‐isolated target cells

Anti‐tumor immunity in b‐lymphocyte‐deprived mice. iii. immunity to primary moloney sarcoma virus‐induced tumors

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