In vitro effects of radiation were studied in two permanent cell lines (AGS and SII) from two patients with adenocarcinoma of the stomach and three permanent sublines from each cell line. Radiation survival parameters for AGS and SII parent cell lines and sublines were determined after in vitro irradiation of their cells with 0.5 to 10 Gy of 60Co gamma rays. The AGS and SII cell lines had different growth properties, DNA contents and radiation survival curves. Surviving fractions of SII parent cells (76 chromosomes) after 2.0 and 10 Gy were 1.22 and 17.8 times greater, respectively, than values for AGS parent cells (47 chromosomes). Sensitivities (D0) were 1.08 and 1.45 Gy for AGS and SII parent lines, respectively. The D0 values for AGS parent cells and sublines were similar (1.01 to 1.08 Gy), but SII parent cells and sublines had D0 values of 1.45, 1.36, 1.37 and 1.12 Gy (for SII-A). Also, the SII parent cells had survival fractions after 2.0 and 10 Gy that were 1.3 and 11.3 times greater, respectively, than values for the SII-A cells. These data show differences in radiation responses among stomach cancer cell lines and sublines that may relate to DNA content, but there was no consistent correlation between radiation response and a particular cell characteristic.
Myeloid leukemia, one of the earliest recognized examples of radiogenic cancer (see Furth and Lorenz, 1954), is conspicuously increased in frequency among people surviving high-level, whole-body ionizing irradiation (Brill et al., 1962; Wald et al., 1962). Because of t,he importance of this neoplasm as a radiation hazard, the mechanisms and kinetics of its induction merit systematic investigation. For this purpose, mice of the R F strain are ideally suited, since a large proportion of them develop myeloid leukemia in response to relatively small amounts of whole-body radiation. Observations on the radiologic and host factors influencing the development of the disease in such animals are surveyed in this article.Clinicopathologic features. The myeloid leukemia encountered in irradiated R F mice is indistinguishable from that occurring spontaneously in mice of this and other strains. Clinical, hematologic, and pathologic features have been described elsewhere (see Dunn, 1954;Upton and Furth, 1954; Parsons et aE., 1962). It is noteworthy, however, that the disease closely resembles chronic granulocytic leukemia of man. The leukocytes in the peripheral blood characteristically show a high degree of maturation, and the infiltrations in the marrow, spleen, and liver are exclusively of granulocytes and their precursors. A predominance of myelocytes and more primitive forms is seen only after serial transplantation of the neoplasm. Whether the clinical course of the primary disease is acute or chronic cannot be determined from the information at hand, since its diagnosis has been made ank rnortem only in terminally ill or moribund mice.Incidence in relation to radiation dose. Apart from the influence of host factors, which is mentioned below, the incidence of leukemia at any given dose level varies with the dose rate; the number and frequency of exposures; the linear energy transfer (LET) of the radiation; and the fraction of the body irradiated.When the mice are exposed to whole-body X or y irradiation in a single, brief exposure ($100 rads/min.) early in adult life (five to ten weeks of age), one finds that the incidence is increased several times above normal by a dose of 100 r, reaches maximal levels at 200-400 r, and declines at higher dose levels, the peak response in males (FIGURE la) exceeding that *Operated by Union Carbide Corporation for the United States Atomic Energy Commission. 189
The insect growth regulator diflubenzuron (DFB), which may also inhibit growth of imaginal epidermal cells in insects, was studied for antitumor activity in two mouse tumor models of epidermal origin. DFB inhibits chitin deposition, but the mechanisms by which DFB controls chitin deposition or regulates growth of insect epidermal cells are unknown. A single injection of 20 mg (800 mg/kg) of DFB into C57BL/6 mice with B16 malignant melanomas or AKR mice with skin tumors (CA 1025) induced a rapid (24 h) decrease in tumor volume in 78% and 66% of the tumors, respectively. In contrast, 85% of the melanomas and 91% of skin tumors in control mice increased in volume during the same 24-h period. Tumor volume decreased by as much as 55% for about 1% of the tumors, but the median decrease was 20% for both types of tumors. Since control tumors concommitantly increased, DFB-treated tumors decreased, relatively, to 60% of the volume of matched control tumors. After the initial volume decrease, both types of tumors resumed exponential growth resulting in an average growth curve delay, calculated for 12-14 days, of about 2.0 days. Subsequent treatment of melanomas with DFB 24 h after the initial treatment resulted in a further decrease in relative tumor volume to 40-50% of control tumor volume and a growth curve delay of 2.6 days. The most effective regimen used was 5 daily, 20-mg doses of DFB. Melanomas decreased to 40% of control tumor volume after the third injection and the mean growth curve delay was extended to 4.3 days.(ABSTRACT TRUNCATED AT 250 WORDS)
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