The
tumors induced in white-lipped marmosets (Saguinus fuscicollis, S. nigricollis) by Rous sarcoma virus (RSV) of chicken origin (RSV-SR) were not transplantable to allogeneic hosts. In contrast, RSV rescued from these
tumors (RSV-M) induced
sarcomas that were transplantable to young but not to adult marmosets. The
tumors induced by RSV-M and the transplants rapidly enlarged, metastasized to various organs, and killed the recipients 29-59 days post inoculation. Cell lines were readily established from all transplantable
sarcomas. No virus expression was detected in transplantable tumor cell lines by electron microscopy or by biochemical and
biological assays. However, RSV of the same subgroup as RSV-SR was rescued from both short-term and long-term
tumor cell cultures by cocultivation with chicken embryo fibroblasts (CEF). The rescued viruses transformed marmoset cells 100-fold more efficiently than CEF cells, although CEF cells remained permissive for virus replication. Cytogenetic studies revealed extensive
chromosome abnormalities in
tumor transplants but not in RSV-M-induced
sarcomas. All cell lines were hyperploid and contained structurally abnormal, large metacentric and telocentric chromosomes. Immunologic studies failed to detect group-specific (gs)
antigen of the
avian sarcoma-
leukemia complex in either RSV-M-induced, transformed cells or
tumor transplants. By
complement-dependent cytotoxicity assays, with the use of marmoset anti-gs serum, RSV-associated
antigen could be detected on the surfaces of
tumor cells. No differences in the expression of this
antigen existed between transplantable and nontransplantable marmoset
sarcomas. All transplantable cell lines contained abnormal amounts of
lipids and
glycogen in comparison to RSV-SR-induced
tumors and normal marmoset cell lines. The
glycogen was associated with unique cytoplasmic membrane complexes and was surrounded by either single- or double-membraned vesicles.