Hematopoietic CFU in mice infected by the polycythemia‐inducing friend virus. I. number of CFU, and differentiation pattern in the spleen colonies

Wendling, Françoise; Tambourin, P; Jullien, P.

doi:10.1002/ijc.2910090312

Cited by 23 publications

(8 citation statements)

References 16 publications

(8 reference statements)

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“…These CFU-S were also shown to produce colonies indistinguishable in their appearance from those produced by normal CFU-S (9,14), which were functionally as competent as the normal in protecting animals from death due to radiation exposure (8, 13, 15, 16), but carried with them a leukemic potential. On the other hand, they differed from normal CFU-S in their seeding efficiency (5,17) and their response to the homeostatic regulators governing organ size (14).…”

Section: Discussionmentioning

confidence: 99%

Effect of antiserum on transplantable hematopoietic colony‐forming units during rauscher leukemia development

1976

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Studies have been carried out to determine the sensitivity of hematopoietic CFU-S from Rauscher leukemic mice to an antiserum against the disease prepared in syngeneic mice. Test of this antiserum against Rauscher virus prior to injection showed it to be effective both in vitro and in vivo. At the same time, normal serum was shown to be without effect either against the CFU-S or against the virus. Spleen CFU-S were obtained from control and leukemic mice over a sequence of days following Rauscher virus injection and assayed by transplantation technique. Prior to transplantation these were incubated in vitro in either normal syngeneic serum or syngeneic antiserum. Incubation with antiserum had no effect on CFU-S obtained from the spleens of normal mice. However, incubation in this antiserum of spleen CFU-S from Rauscher leukemic mice resulted in a reduction of up to 50% in their colony-forming ability. Additional tests with guinea pig complement suggested that the levels of inactivation seen are not complement limited. This antiserum-induced reduction in colony formation was first evident in the second week after the injection of virus, coincident with the onset of splenomegaly in the leukemic mice. Thereafter, sensitivity of CFU-S to the antiserlm could be detected up to the terminal point of the leukemia (44 days).

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Section: Discussionmentioning

confidence: 99%

Effect of antiserum on transplantable hematopoietic colony‐forming units during rauscher leukemia development

1976

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“…With the knowledge that preleukemia in other MuLV systems may be associated with changes in the expression of viral (e.g., xenotropic MuLV gp70) and host (e.g., H-2 and Thy 1.2) cell surface antigens (6,8,24) and with the knowledge that FV-infected mice (25) and in vitro bone marrow cell cultures (26) either contain increased numbers or sustained proliferation ofpluripotent hemopoietic stem cells (CFU-S), we were desirous to know if the spleen cells obtained from SFFV ÷ mice expressed any detectable alteration in membrane surface markers. We elected to conduct cell transplantation studies because this would allow us to enumerate the frequency of CFU-S per SFFV + spleen, the transplantability of such cells, and their ability to protect lethally irradiated mice from hemopoietic death.…”

Section: Rejection Of Sffi~ Preleukemic Spleen Cells By Nonimmunized mentioning

confidence: 99%

Persistence and pathogenicity of defective Friend spleen focus-forming virus. Decreased transplantability of hemopoietic cells as a marker for preleukemic change.

Eckner¹,

Hettrick²

1979

The Journal of Experimental Medicine

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A latent form of persistent infection can be established in susceptible adult mice inoculated with a preparation of defective Friend spleen focus-forming virus (SFFV) purified free from standard leukemia-inducing helper virus (LLV-F). SFFV persistence was initially observed using an in vivo rescue technique in which SFFV could be directly rescued to form splenic foci of malignant erythropoiesis in mice. At approximately 30 d after virus inoculation however, SFFV could not be rescued after inoculation of LLV-F indicating that persistently infected (i.e., SFFV+) mice were either immume to exogenous helper virus or able to express SFFV-associated defective-interfering (DI) function(s). Persistent infection by SFFV was further documented using an in vitro rescue technique and ultimately resulted in the induction by SFFV of erythroleukemia in the absence of polycythemia or overt virus production. However, SFFV rescued by LLV-F from persistently infected normal and transformed hemopoietic cells was able to induce polycythemia in adult mice suggesting that this is a helper controlled property of the Friend virus complex. Transplantable SFFV-induced erythroleukemic cells could be retrieved from persistently infected yet histologically normal mice. The duration of SFFV persistence in normal spleen tissue suggests that the SFFV provirus resides in either a long-lived or pluripotent hemopoietic cell. Further, certain changes occurred, presumably in the membranes of persistently infected cells, which preceded the overt development of Friend leukemia and facilitated the definition of an SFFV preleukemic phase. Cell surface alterations were revealed using cell transfer techniques. Hemopoietic cells harboring a rescuable SFFV failed to proliferate when inoculated into lethally irradiated, syngeneic adult mice. In contrast, the transformed progeny of preleukemic cell populations and spleen cells transformed by FV complex (i.e., cells replicating both SFFV and LLV-F) were not rejected. This result suggests that histologically normal SFFV+ preleukemic cells express an antigen recognition site which is not present on overtly transformed cells and which may be a pertinent surveillance target for host anti-leukemogenic reactions.

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“…Cell suspensions from normal or leukemic spleens were prepared by the usual method (Wendling et al, 1972). The number of nucleated cells in the samples was determined using a hemocytometer.…”

Section: Preparation Of Cell Suspensions and Spleen Colony Assaymentioning

confidence: 99%

“…However, the IV injection of leukemic spleen cells into histocompatible irradiated recipients gives rise . to splenic colonies resulting from the proliferation and differentiation of the grafted hematopoietic stem cells (Wendling et al, 1972).…”

Section: Cytofoxic Activity Of Antisera Against Spleen C5bny Cells Dementioning

confidence: 99%

“…On the basis of cytogenetic experiments, evidence was presented that Friend leukemic cells were not transplantable (Takada et al, 1971). Moreover, extensive investigations of colonies developing in the spleens of heavily irradiated hosts grafted with spleen cells from FLVinfected leukemic donors have convinced us of the rare occurrence of tumor colonies, at least during the first month after FLV infection (Wendling et al, 1972(Wendling et al, , 1973.…”

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confidence: 99%

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Oncogenicity of friend‐virus‐infected cells: Determination of origin of spleen colonies by the H‐2 antigens as genetic markers

Wendling¹,

Tambourin²

1978

Intl Journal of Cancer

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Spleen cells from mice infected with Friend leukemia virus (FLV) inoculated by the intravenous route give rise to macroscopically visible colonies in the spleens of normal F1 histocompatible hybrid hosts. A study of H-2 antigens as generic markers for identification of strains of origin of cells constituting the spleen colonies was undertaken. The standard cytotoxic test was demonstrated to be suitable for characterizing the H-2 antigens present on the surface of spleen cells from normal of FLV-leukemic parents of F1 hybrid mice. Individual colonies dissected out of the spleen of (C3HxC57B6/6) F1 recipients (H-2k/H-2b), 10 days after the intravenous graft of FLV-infected spleen cells of C3H origin (H-2k), were all sensitive to anti-C57BL/6 antibodies. In the same way, colonies obtained from the spleens of (DBA/2xC57BL/10) F1 recipients (H-2d/H-2b) grafted with DBA/2 leukemic spleen cells (H-2d) were all sensitive to both anti-H-2b and anti-H-2d antibodies. These results directly prove that the main cell population constituing a spleen colony arises from the recipient. The authors conclude that the spleen colonies do not result from the neoplastic proliferation of injected donor cells but rather from the multiplication of host cells transformed by Friend virus produced by the grafted cells.

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Hematopoietic CFU in mice infected by the polycythemia‐inducing friend virus. I. number of CFU, and differentiation pattern in the spleen colonies

Cited by 23 publications

References 16 publications

Effect of antiserum on transplantable hematopoietic colony‐forming units during rauscher leukemia development

Effect of antiserum on transplantable hematopoietic colony‐forming units during rauscher leukemia development

Persistence and pathogenicity of defective Friend spleen focus-forming virus. Decreased transplantability of hemopoietic cells as a marker for preleukemic change.

Oncogenicity of friend‐virus‐infected cells: Determination of origin of spleen colonies by the H‐2 antigens as genetic markers

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