Hamster Tumor Cells Research Articles

The SV40 S antigen; a carcinoembryonic-type antigen of the hamster?

AbstractIn addition to hamster tumor cells induced or transformed by SV40, hamster anti‐SV40 S (Surface) antiserum also reacted with non‐SV40‐exposed cell lines spontaneously induced (BHK 21) or transformed by heterologous oncogenic DNA and RNA viruses in the indirect membrane fluorescent antibody test. The antiserum titered equally with both BHK and SV40‐transformed cells and the reaction could be absorbed with either of these cell lines, or with hamster embryo. The antiserum also reacted with early hamster embryo cells, although various organ cells from late fetuses, newborns and adults were negative. Mouse cell lines spontaneously induced (BALB/c‐3T3) or transformed by SV40 and adenovirus 12 were also non‐reactive. The results suggest that the antigen in question is a hamster somatic antigen present during embryonic life and derepressed in lines of actively growing cells.

Effect of cyclophosphamide on syngeneic transplantation of para-adenovirus-7-transformed tumor cells in hamsters.

AbstractThe effect of cyclophosphamide on the transplantability of hamster tumor cells transformed by PARA‐adenovirus 7 was investigated. Normally, such syngeneic transplants seldom, if ever, regress spontaneously. It was found that chemotherapy was remarkably effective against this neoplasm. A single inoculation of the drug (200 mg/kg) prevented the growth of 104‐105 transplanted cells, and promoted regression of palpable tumors. Weekly drug inoculations prolonged the survival of hosts bearing large neoplasms. Animals successfully treated proved to be resistant to subsequent tumor‐cell challenge. The chemical did not prevent tumor growth if given prior to the transplant. There is suggestive evidence that host tumor resistance may have contributed to the success of cyclophosphamide therapy.

Rescue of the genome of the defective murine sarcoma virus from a non-producer hamster tumor cell line, PM-1, with murine and feline leukemia viruses as helpers.

AbstractSome properties of a hamster tumor cell line, the PM‐1 cl 6 (PM‐1), derived from a hamster tumor induced by the Harvey murine sarcoma virus (H‐MuSV) are described. The PM‐1 cell line appears to be free of viruses of the murine leukemia‐sarcoma complex as tested by the absence of plaque formation in the mixed cytopathogenicity test for MuLV, the absence of gs‐antigen (s) of MuLV demonstrated by the indirect immunofluorescence technique and the lack of focus formation in MuSV‐sensitive 3T3 cells. Incorporation studies with 3H‐uridine have shown lack of production of viral particles in the density region 1.16 g/cm3, and cell‐free preparations of the PM‐1 cells were not sarcomagenic in hamsters. Rauscher and Gross MuLV as well as MuLV isolated from several chemically‐induced murine leukemias were able to rescue the MuSV genome from the PM‐1 cells as demonstrated by focus formation of the different pseudotype MuSV in 3T3 cell cultures as well as sarcoma induction in mice. Trans‐species rescue of the defective MuSV genome has also been accomplished with feline leukemia virus (FeLV) as helper. The rescued pseudotype MuSV (FeLV) produced foci in feline embryonic cell cultures. The PM‐1 cell line should be useful for further studies of mammalian viruses of the Oncorna group.

The response of BHK21 cells to infection with type 12 adenovirus: VI. Synthesis of virus-specific RNA

When G1-arrested BHK21 cells are infected with type 12 adenovirus (Ad12), some of the newly synthesized RNA is virus specific. RNA-DNA hybridization-competition experiments have demonstrated that this RNA corresponds to up to 60% of those “early” mRNA sequences which are transcribed in productively infected human embryonic kidney (HEK) cells. No “late” Ad12 mRNA was detected in BHK21 cells. Comparison of Ad12-specific RNA sequences transcribed in Ad12-infected BHK21 cells and in Ad12-induced hamster tumor cells (line HT 2) by hybridization-competition reaction indicated that no virus-specific sequences are transcribed in HT 2 cells which are not also present in BHK21 cells abortively infected with Ad12. Attempts to detect any Ad12 DNA synthesis in BHK21 cells by DNA-DNA hybridization, under conditions of minimal background cellular DNA synthesis, were unsuccessful. Correspondingly, immunofluorescent staining experiments failed to detect Ad12 capsid protein synthesis in over 10 4 infected cells.

Properties of a murine sarcoma virus isolated from a tumor arising in an NZW-NZB F 1 hybrid mouse. II. Physical and biological characteristics.

AbstractThe properties of a potent murine sarcoma virus (MSV), which was isolated after in vivo passage of a spontaneous tumor arising in an NZW/NZB F1 hybrid mouse, are described. The agent had the morphological and growth characteristics of a type C virus, and contained the group‐specific (gs) antigen of the murine leukemia‐sarcoma viruses. The virus induced discrete, focal lesions of transformed cells in mouse tissue‐culture cells. Focus formation usually followed a “two‐hit” titration pattern, and sarcoma virus preparations contained a large excess of an accompanying non‐transforming type C virus. The MSV was stable when stored at — 70° C; it was ether‐sensitive and had a buoyant density of 1.16g/cm3 when centrifuged in sucrose density gradients. These properties are similar to those of the Moloney (M‐MSV), Harvey (H‐MSV), and Kirsten (Ki‐MSV) isolates of MSV. When inoculated into hamsters, the new strain of MSV rapidly induced sarcomas. While the viruses produced by hamster and mouse tumors both contained the murine gs antigen, the host range of the MSV was altered by hamster passage. It failed to induce focal lesions in mouse and hamster cells, and did not induce sarcomas or leukemias when injected into newborn mice and hamsters. The antigenic properties and infectivity of the virus produced by hamster tumor cells were significantly different from the properties of the hamster leukemia pseudotype viruses obtained from hamster tumors induced by the other strains of MSV.

Cytochemistry, cytogenetics and ultrastructure of hamster tumour cells carrying mouse sarcoma viral genome (HT-1 cells).

The pleomorphic cytology of the HT-1 cell line is described. Cytochemical studies indicated the presence of glycogen and lysosomes in these cells. Cytogenetic studies demonstrated the presence of a large telocentric chromosome (M1) and two minute chromosomes (M2) not found in normal hamster cells. A cloned line was isolated which did not contain these marker chromosomes. All cells were hyperdiploid with chromosome number around triploidy, although none was a true triploid. Ultrastructural studies revealed the presence of "nuclear bodies", "dense bodies" and "interchromatinic granules" which have been previously described in viral induced malignancies. A few of the cells contained in their cytoplasm structures of approximately 700 [unk] in diameter which bore some resemblance to immature virus particles. Both light and electron microscopy demonstrated some nuclei lacking chromatin aggregates. This is interpreted to mean that the total genetic material of these nuclei was dispersed as free DNA not linked with histone to form chromatin aggregates.

Presence of sarcoma genome in a "non-infectious" mammalian virus.

Virus particles, antigenically related to mouse sarcoma virus, can be induced from hamster tumour cells. They are “defective” in their failure to replicate in or transform hamster, mouse or rat cells, although they contain viral-specific RNA and, with “helper” mouse leukaemia virus, show sarcomagenic activity.

Variations in Immunogenicity of Disrupted Cells Prepared From an Adenovirus-7 Hamster Tumor Cell Line<xref ref-type="fn" rid="FN2">2</xref>

Variations in Immunogenicity of Disrupted Cells Prepared From an Adenovirus-7 Hamster Tumor Cell Line<xref ref-type="fn" rid="FN2">2</xref>

Detection of Avian Leukosis Viruses in Chickens by an in Vivo Rous Sarcoma Virus Genome Rescue Test

The presence of avian leukosis virus(es) in sera of chicks from commercial flocks can be detected by the Rous sarcoma virus (RSV) genome rescue test, which involves injection of BH-RSV HTC (RSV-transformed hamster tumor cells) two to three weeks after injection of the suspect material into leukosis-free chicks. Appearance of tumors in the recipient chicks is indication of the presence of ALV in serum and correlates well with Cofal tests.

Transformation and productive infection of human osteosarcoma cells by a feline sarcoma virus.

FELINE sarcoma virus (FSV) transforms human embryo cells in vitro1; it therefore seemed interesting to determine whether this virus could transform human osteosarcoma cells. Defective Moloney sarcoma virus genome can be rescued from non-producer hamster tumour cells by feline leukaemia virus (FeLV)2 and because FSV stocks also contain excess FeLV (ref. 1 and unpublished observations of R. V. G.), it was hoped that human osteosarcoma cells transformed by FSV and co-infected with FeLV might yield a human sarcoma virus.

Chromosome, transplantation and tumour antigen studies of three virus-induced tumour cell lines.

The transplantability to adult hamsters, the CF titers of tumour antigen and the chromosome content was determined at a single passage level for two established adenovirus 12-induced hamster tumour cell lines and an SV40-virus tumour cell line. The cell lines had been passaged more than 200 timesin vitro, and immunofluorescent tests showed that all the cells contained specific virusinduced tumour antigen. The SV40 cell line and one of the adenovirus 12 tumour cell lines (TAd III cells) were transplantable to adult hamsters. The second adenovirus 12 tumour cell line (H212 cells) did not produce tumours in adult hamsters, but produced tumours in new-born hamsters. TAd III cells contain relatively a low CF titre of tumour antigen while H212 cells contain high CF titres of antigen. Cytogenetic analysis showed that all tumour cell lines were markedly different from normal hamster cells. The incidence of marker chromosomes was greatest for SV40 tumour cells, and smallest for H212 cells. The results of cytogenetic and antigen studies are discussed in relation to the transplantability of the tumour cell lines.

Rescue of murine sarcoma virus genome in mixed cultures of 'non-producer' hamster tumour cells and helper virus carrier cell lines.

Microbiology Society journals contain high-quality research papers and topical review articles. We are a not-for-profit publisher and we support and invest in the microbiology community, to the benefit of everyone. This supports our principal goal to develop, expand and strengthen the networks available to our members so that they can generate new knowledge about microbes and ensure that it is shared with other communities.

SV 40誘発腫瘍細胞の長期培養による変化について

SV 40誘発腫瘍細胞の長期培養による変化について

Fetal Antigen Capable of Inducing Transplantation Immunity against SV40 Hamster Tumor Cells

Abstract Hamster, mouse and human cells transformed by simian virus 40 (SV40) share a common antigen capable of stimulating specific transplantation immunity against SV40-induced tumors in hamsters (1, 2). Cursory consideration of this observation might suggest that the viral genome must code for the common tumor-specific antigen in the different cell species. Knowledge acquired recently about the size of the SV40 genome limits the potential informational complement of this virus to seven to eight genes (3). Available data indicate that at least six genes are required for virus synthesis (3, 4), and radiation studies suggest that one or two different genes are required for transformation (5). It is becoming increasingly difficult to adhere to the concept that the virus codes directly for the tumor-specific transplantation antigen (TSTA) which is incorporated into the membrane of transformed cells unless the TSTA is a small protein and is a pleiotropic viral gene product.

Isolation of a variant strain of Rous sarcoma virus oncogenic for ducks and mammals.

In contrast with the Schmidt-Ruppin strain of RSV, Bryan strains are not oncogenic for ducks. From the Bryan standard strain (BS-RSV) a variant virus oncogenic for ducks was isolated by passing BS-RSV through cortisone-treated ducklings together with chick embryonic tissues. From the Bryan high titer strain (BH-RSV) such a variant virus could not be isolated. The variant virus (BK-RSV) is also oncogenic for mice and hamsters, whereas parent strain lacks such oncogenicity for mammals. Thus, there may be some correlation between oncogenicity for ducks and mammals. Mouse or hamster tumors induced by the BK strain did not produce infectious RSV eitherin vivo orin vitro. However, when hamster tumor cells in appropriate amounts were inoculated in the wing web of chickens, sarcomas were induced yielding infectious RSV. Thus, the RSV genome persists in BK-induced mammalian tumor cells and is able to produce infectious virus in the presence of chicken cells.

Demonstration of a tumour and transplantation antigen in hamster tumours induced by an avian adenovirus (CELO).

Tumour transplant immunity studies in hamsters demonstrated a transplantation antigen in CELO tumour cells. The transplant immunity was apparently virus specific since hamsters immunized with CELO virus did not reject transplants of SV40 induced hamster tumour cells. Immunofluorescence studies indicated the presence of a CELO virus tumour antigen in serially cultured tissue culture cells derived from a CELO induced hamster tumour. The antigen was located in the cell nuclei, and could not be detected in the cytoplasm. CELO virus has several properties which may make it a useful model virus for studies of viral oncogenesis.

Trans-species rescue of defective genomes of murine sarcoma virus from hamster tumor cells with helper feline leukemia virus.

This report describes a trans-species rescue of defective MSV genome with helper leukemia virus derived from cats. This rescue was achieved by in vitro co-cultivation of hamster tumor cells with feline embryo cells in the presence of helper feline leukemia virus (FeLV), or by inoculation of tumor cells into FeLV-infected newborn cats. The rescued focus-forming viruses produced foci in feline embryo cultures but not in cultures of mouse, rat, and hamster species. One isolate was tested and found to induce sarcoma in a kitten. Antigenic and viral interference studies indicated that the focus-forming virus has the viral envelope of FeLV. Virus stocks consisted of a mixture of focus-forming particles and a 1000-fold excess of helper FeLV. Virus assay pattern in feline embryo cultures with or without added helper FeLV indicated that this helper virus is required for the transformation of feline cells.

Rescue of Defective Murine Sarcoma Virus Genome From 50 Clones of a Nonproducer Hamster Tumour Cell Line

A cell line (HT-1) derived from a hamster tumour induced by the Moloney sarcoma virus has been extensively used for preparation of murine pseudotype sarcoma viruses (Huebner et al. 1966; Hartley et al. 1969). Infectious virus could not be isolated from these cells nor was the group specific (gs) antigen of the murine C-type RNA viruses detectable in complement-fixation tests (Huebner et al. 1966). In further studies with this cell line, clonal sublines were derived and tested for infectious virus and virus particle production, gs antigen using both complement-fixation and precipitation-ingel assays, and the presence of virus genome by a highly reproducible rescue technique. HT-1 cells in the 80th in vitro passage were seeded into ten 60 × 15 mm. plastic Petri dishes (50 cells/dish). Each culture yielded 5 to 10 individual colonies, of which five were isolated by trypsinization within glass cloning rings. Each of the 50 clones was maintained separately in Eagle’s basal medium with 10% foetal bovine serum.

Induction of tumor-specific transplantation immunity in hamsters with cell fractions from adenovirus and SV40 tumor cells.

SummaryThe specific induction of transplantation immunity against adenovirus 31-and SV40-induced hamster tumor cell challenge employing either a crude membrane fraction of homologous adenovirus 31 tumor cells or SV40 tumor cell fragments is described. In each case immunity was equivalent or superior to that induced by whole, irradiated tumor cells previously described to contain TSTA, or to that induced by vaccination of mature hamsters with the live virus. Whole tumor homogenate of adenovirus 31 hamster cells, from which the membrane fraction was obtained failed to induce TSTA immunity. The possibility exists that a masking or enhancing component is present in the homogenate to interfere with TSTA immunity induction or detection.Addendum. Hamsters immunized with SV40 tumor cell ghost lysates were uniformly resistant to an initial cell challenge as shown in Table III. Several months later the survivors were challenged a second time and 42% of the hamsters developed tumors by day 50. One hundred percent of...

Electron Microscopic Observations on the Association of Viruses With Membrane Systems in Hamster Tumor Cells Propagated in Tissue Culture<xref ref-type="fn" rid="FN2">2</xref>

Electron microscopic observations on several cell lines derived from hamster tumors, induced by inoculations of Bryan strain Rous sarcoma virus, confirmed the presence of a reovirus (Type III) and indicated two other types of “virus-like” particles. The reovirus was observed in large cytoplasmic viroplasms. Particles with morphology similar to the reovirus particles passed through the outer membrane of mitochondria lying close to the reovirus viroplasms. The particles acquired α membrane envelope in this manner. Particles were not seen in the matrix of the mitochondria. The two other types of virus-like particles observed were 1) α “budding” particle, approximately 155 m/μ in diameter, which originated from electron-dense condensations at the plasma membranes of the cells in vitro, and 2) another budding particle previously described, with radial configuration of internal material that originated from the endoplasmic reticulum. Biologic significance has not been ascribed to these latter two particle types; however, they exhibit the basic criteria for viruses. They appear as accumulations of abnormal or altered protein or nucleoprotein. These observations suggest the possibility of new agents which may be endemic in the hamster.