In vitro studies on oral postoperative adjuvant chemotherapy of uterine cervical cancer.
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In order to improve the postoperative survival rate of patients with cervical cancer, we have treated them with adjuvant chemotherapy (oral Tegafur) and proved this treatment to be useful. However, the mechanism of recurrence during oral adjuvant chemotherapy is not yet known.<BR>In this study, first, a cell line originating from a squamous cell carcinoma of the uterine cervix (SKG-IIIb) was cultured in a medium containing a comparatively low dose of 5-fluorouracil (5-FU), and the morphological changes, proliferating activity, 5-FU sensitivity and DNA metabolism of cancer cells were examined.<BR>A subline (SKG-IIIbR) which could proliferate in a medium containing 0.1 μg/ml of 5-FU was obtained after about 30 months of culture.<BR>There was no significant difference in light microscopic findings between SKG-IIIb and SKG-IIIbR. However, SKG-IIIbR grew relatively slowly in the medium containing 5-FU, with a population doubling time of 154 hours.<BR>The EC50 (Effective Concentration for 50% Cell Kill) of 5-FU on SKG-IIIb and SKG-IIIbR cells after 96 hours of incubation with 5-FU was calculated by growth inhibition assay to be 2.6 μg/ml and 3.6 μg/ml, respectively.<BR>The incorporation of 3H-deoxyuridine and 3H-thymidine into the DNA of SKG-IIIb and SKG-IIIbR cells after 96 hours of incubation with 5-FU was assayed by the method of Ball, et al.<BR>The incorporation of deoxyuridine was inhibited at 0.1 to 10.0 μg/ml of 5-FU in both cells. On the other hand, the incorporation of thymidine was not inhibited even at 1.0, μg/ml of 5-FU in SKG-IIIbR, although it was inhibited at 0.1 μg/ml of 5-FU in SKG-IIIb.<BR>The following conclusions were drawn : <BR>1) The proliferating activity of cancer cells decreased under longt erm treatment with a comparatively low dose of 5-FU.<BR>2) Cancer cells did not easily become resistant to 5-FU, but were not totally killed by this treatment.<BR>3) The cells appear to react by increasing phosphorylation of thymidine in the salvage pathway of DNA metabolism, which may be one of the factors causing survival or regrowth of cancer cells during 5-FU treatment.
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