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Biomedical subjects

G Andersson

Publications and source records attributed to G Andersson.

At least 343 records · Page 19Linked to original sources
PubMed1977

Accumulation of polyploid cells and G2-phase cells during ascites tumor growth.

Ehrlich ascites tumor cells from the plateau phase of growth were transplanted into new hosts, pulse-labeled with tritiated thymidine and blocked with repeated injections of vinblastine. When unlabeled cells were analyzed for their cellular DNA content utilizing a cytophotometric technique it was found that in relation to the total number of cells (labeled plus unlabeled), 13% had a 2C DNA content, 36% a 4C DNA content and 5% and 8C DNA content at 0.5 hours after tranplantation. By 24 hours the distributions changed dramatically: the initally unlabeled 2C cells were now 4C, the 36% of the cells that were initially 4C partitioned into 24% that were still 4C and 12% that progressed to 8C, and the initial 8C cells remained 8C. These studies indicate that the accumulation of 4C cells during the plateau phase of growth is due to a combination of G2 diploid and G1 tetraploid cells.

Animals↗
PubMed1977

Population kinetics of an Ehrlich ascites tumor following treatment with methylglyoxal-bis(guanylhydrazone), a polyamine synthesis inhibitor.

Population kinetics of Ehrlich ascites tumor cells grown in vivo were studied following treatment with methylglyoxal-bis(guanylhydrazone) (MeGAG; NSC-32946), a potent chemotherapeutic agent and a specific polyamine synthesis inhibitor. MeGAG-treatment resulted in a continuous accumulation of cells in the S and G2 phases of the cell cycle, and, as a consequence, the rate of cell proliferation decreased. This finding emphasizes the importance of the polyamines for progression through the cell cycle.

Adenosylmethionine Decarboxylase↗
PubMed1977

Kinetics of cell proliferation and polyamine synthesis during Ehrlich ascites tumor growth.

The kinetics of cell proliferation and polyamine synthesis during Ehrlich ascites tumor growth were studied. The steady deceleration of the specific growth rate with increasing tumor mass that was observed was attributable to a prolongation of the cell cycle, particularly of the S and G2 phases. The cell cycle time (Tc) was 43.3 hr (TG1 equals 10.8, TS equals 26.8, and TG2 equals 5.7 hr) on the seventh day of growth and 76.0 hr (TG1 equals 14.0, TS equals 52.0, and TG2 equals 10.0 hr) on the tenth day of growth. The growth fraction showed a decrease from 0.77 to 0.60 during the 7- to 10-day tumor growth interval. The cell death rate remained low and essentially unchanged during this period. A high correlation was found between polyamine synthesis (ornithine decarboxylase activity) and the specific growth rate; the correlation coefficient was 0.985. There was also a high positive correlation between the cellular polyamine (spermidine and spermine) and nucleic acid content (spermidine: DNA equals 0.916, spermine: DNA equals 0.947, spermidine:RNA equals 0.907, and spermine: RNA equals 0.881). These observations suggest that there may be a functional coupling between polyamines and nucleic acids, and they support the hypothesis that polyamines play an important role in DNA replication and cell division.

Animals↗
PubMed1976

Increase in the amount of nuclear RNA in liver of ascites tumour-bearing mice.

The effect of tumour growth on the liver of the host was studied in the Ehrlich ascites tumour system. During the experimental period there was no infiltration of tumour cells in the liver, and the increase in the proliferation rate of Kupffer cells and parenchymal cells was only small. An increasing stability of the liver cell nuclei towards disruption during the isolation procedure was found to accompany the ascites tumour growth. In parallel, there was an increase in the amount of nuclear RNA and in the cellular speridine concentration. The major cause of these changes is probably an increasing demand on the liver by the growing tumour, illustrated by the fact that an amount of protein exceeding that of the whole liver accumulates in the ascites fluid during tumour growth. A hypothesis according to which the cellular accumulation of spermidine may be involved in the stabilization of cell nuclei and in the accumulation of nuclear RNA is advanced.

Animals↗