DMSO-induced terminal differentiation and trisomy 15 in myeloid cell line transformed by the Rauscher murine leukemia virus.
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Biomedical subjects
Publications and source records attributed to M Vermey.
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Cell proliferation was investigated in normal and Rauscher Leukemia Virus-infected BALB/c mice. Five days after inoculation, islands of leukemic blasts arose in the red pulp, and proliferated as shown by autoradiographic analysis after a pulse of 3H-Thymidine. These cells subsequently infiltrated the whole spleen and 3 weeks after infection about 60% of the spleen consisted of large immature erythroblast-like cells. Repeated injections of 3H-Thymidine led to uniform labeling of 85% of the spleen cells. Cell cycle analysis showed that for bone marrow as well as for spleen cells the total duration of the cell cycle did not differ from the cell cycle times of normal erythroblasts. From the difference between the actual doubling time and the potential doubling time (estimated on the basis of the cell cycle time) it can be calculated that considerable cell loss must occur. This cell loss is only to a minor extent due to the release of blasts into the peripheral blood. Probably cell death and extrusion of nuclei during erythroid differentiation are the main factors involved.
The regeneration capacities of normal and transposed small bowel epithelium were compared in rats after applying high doses of X-irradiation. It has been shown that the potency of the mucosa to regenerate is much higher than assumed and that the mucosa can regenerate after single doses varying from 2000-5000 R. Even in the villus epithelium and in flat epithelium covering infiltrates of the lamina propria cells survive, which are still able to resume proliferative activity several days after irradiation.