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PubMed1980

Influence of tumour volume and cell kinetics on the response of the solid Yoshida sarcoma to hyperthermia (42 degrees C).

The cytokinetic response of the solid Yoshida sarcoma to hyperthermia was examined at two tumour volumes, 1.0-1.5 ml and 3.0-3.5 ml. The tumour, growing on the feet of rats, was heated at 42 degrees C for 1 h by water-bath immersion. The larger tumour grew more slowly than the smaller one (doubling time 144 h vs 36 h) due to a halving in growth fraction from 67.8 to 39.6% and an increase in cell-loss factor from 59 to 75.9%. Cell cycle and phase times were similar at both volumes. The effect of heat on the population kinetics at both volumes was similar but complex, and involved delayed cell death after up to 10 mitoses. Initial cell killing and blockade of cell-cycle progression (0-24 h) was followed by recovery of proliferation due to recruitment of cells from the non-proliferative compartment, cell cycle and phase times remaining unaltered. From 48 h, the proliferation rate declined progressively, and tumours were completely necrotic 7-8 days after heat. The damaging effects of heat were at least as severe in the large tumours with a low labelling index and small growth fraction as in the smaller tumours with a much larger compartment of proliferating cells and shorter doubling time. The results imply that there may be no simple relationship between proliferative status and thermosensitivity of a tumour, and illustrate the difficulty in predicting tumour response to heat on the basis of cytokinetic studies.

Animals↗
PubMed2002

Cancer-related anemia in a rat model: alpha2-macroglobulin from Yoshida sarcoma shortens erythrocyte survival.

Implantation of Yoshida ascites sarcoma in rats was found to lead to a reduction in the hemoglobin content, the erythrocyte count and the packed cell volume of blood to 30% of normal in 4 d; however, there was no decrease in the mean cell hemoglobin, the mean cell volume and the mean corpuscular hemoglobin concentration, or suppression of erythropoiesis. The red cells from the circulation of tumor-bearing animals, tagged with (51)Cr and injected intravenously in normal rats, showed significantly faster clearance than normal. The erythrocytes contaminating the tumor ascites exhibited extremely short survival, suggesting that one or more secreted tumor product(s) may be responsible for the effect. Incubation of red cells from normal rats in the cell-free ascites fluid, or with an isoform of alpha2-macroglobulin purified from it, also led to reduction in the survival; but the ascites fluid depleted specifically of alpha2-macroglobulin was without any effect. The erythrocytes exhibiting reduced survival showed a proportionate decrease in their cellular deformability. The study identifies a tumor product that is directly responsible for the causation of anemia in the host, and the mechanism by which it does so.

Anemia↗
PubMedDate not supplied

The possible role of stromal influences in tumor cell heterogeneity. Histology and fibronectin pattern of the Yoshida sarcoma of the rat.

Yoshida tumors implanted subcutaneously in the rat are conspicuously heterogeneous. A definite zoning can be discerned. Cell nuclei range from uniform epitheloid (type I) via pleomorphic (type II) to compact (type III). Type III is seen to detach at the rim of the tumor and to infiltrate the dermis. Type I is characterized by positive pericellular fibronectin staining, type II and III are fibronectin-negative. A marked spatial relationship was seen between types II and III on one hand and the presence of collagenous stroma on the other. It is conjectured that stromal components play a role in tumor promotion or progression.

Animals↗