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Morphologic changes were studied in 43 rats that were paralyzed by an epidural fibrosarcoma inoculated through the spinous process. By this technique, of 29 rats examined radiographically, the tumor destroyed vertebral bone in 22. Changes of the cord in the early stage of paralysis were specially analyzed by Marchi's stain and microangiograms. In compromised cord segments in the early stage, extravasation of contrast medium was observed in the gray matter and the dorsal funiculus; and in the dorsal funiculus just proximal or distal to the compressed portion, hemorrhagic areas were present. Ascending degenerated fibers in the dorsal funiculus, which were derived from the degenerated posterior nerve root or the degeneration of the dorsal funiculus in the compressed segments, were characteristically detected in rats in the early stages. In the advanced stages a transverse cord lesion was observed at the involved level. Based on the present analyses, to prevent more advanced damage to the spinal cord, the tumor should be removed at an early stage that clinically coincides with the period when radicular signs appear.

Murine oncovirus antigens represent excellent targets for immune recognition, and virus-associated tumors are generally susceptible to various immunotherapy protocols. Virus-negative tumors, however, are nonimmunogenic and refractory to immunologic control. Therefore, the feasibility of the introduction of antigens onto non-virus-expressing tumors in situ in inbred C57BL/6J mice by systemic administration of nononcogenic murine retroviruses was investigated. Two classes of murine fibrosarcomas were studied: a 3-methylcholanthrene-induced fibrosarcoma syngeneic to C57BL/6 mice (MCA-FS) and a Harvey murine sarcoma virus-transformed, nonproducer fibrosarcoma syngeneic to C57BL/6 mice (H-NP). Both were found to be devoid of infectious ecotropic murine leukemia virus (MuLV) or MuLV antigens. A single dose of Friend murine leukemia virus (F-MuLV) was used to superinfect MCA-FS- and H-NP-induced tumors in vivo and converted these tumors to a highly productive, virus-positive state. In vivo superinfected tumors were indistinguishable from their preinfected counterparts by competition radioimmunoassays for the virion's major envelope glycoprotein, gp71, and its group-specific antigen, p30, and by assays for infectious virus. Analysis of virus from tumor extracts proved that the antigenic specificity of the superinfected tumor was provided by F-MuLV administered systemically to the animals. Finally, an immunoperoxidase technique, applied to tumor cross sections, demonstrated the uniform appearance of viral antigens in the superinfected tumors.

The effect of an i.p. injection of glucose on the thermal response of murine tissues was studied. Animal tumors were early generation isotransplants of a spontaneous fibrosarcoma, FSa-II. Tumors were transplanted into the foot pad, and hyperthermia was given by immersing the foot into a constant-temperature water bath. The tumor and normal tissue responses were studied by assays of the time required for half the tumors to reach 1000 cu mm from treatment day and of the treatment time required for one-half of the animals to develop a loss of one toe or greater reaction. The glucose administration enhanced tumor response more substantially than normal tissue response. The enhancement was greater for a large tumor than for a small tumor and also greater at 42.0 degrees than at 45.5 degrees. Presumably, the hyperglycemia induced acidosis which eventually enhanced thermal response. Present results suggested that the hyperglycemia is a potential method to specifically enhance tumor response at elevated temperatures.