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Biomedical subjects

M Ikenaga

Publications and source records attributed to M Ikenaga.

At least 127 records · Page 7Linked to original sources
PubMed1983

Increased sensitivity of cultured fibroblasts from colon cancer-prone rats to cytotoxicity of carcinogens and to viral transformation: a comparison with fibroblasts from patients with adenomatosis coli.

Lethal effects of mitomycin C (MMC), 4-nitroquinoline 1-oxide (4NQO) and ultraviolet light (UV) on fibroblast cell lines derived from a colon cancer-prone substrain of Wistar-Furth rats (WF/OSAKA rats) were measured in terms of the cellular colony-forming ability, and compared with the sensitivity to these agents of human fibroblasts from patients with adenomatosis coli and rectum (ACR). All 6 fibroblast strains from the cancer-prone WF/OSAKA rats were significantly more sensitive (though to various extents) to MMC as well as 4NQO than normal rat fibroblasts derived from the parental WF Hiroshima rats. These WF/OSAKA cell strains were slightly more sensitive to UV than normal rat cell strains. Similarly, 5 out of 6 fibroblast strains derived from ACR patients were hypersensitive to both MMC and 4NQO. Further, the WF/OSAKA cell strains were more susceptible to morphological transformation induced by Kirsten murine sarcoma virus than normal rat strains. The observed higher sensitivity to chemical agents and to viral transformation suggests a close similarity in cellular terms between the colon cancer-prone WF/OSAKA rats and human individuals affected with ACR.

4-Nitroquinoline-1-oxide↗
PubMed1982

[TAC-278. A new 5-FU derivative, by the oral route for its efficacy and safety in 36 patients with advanced cancers].

Tumor regression was observed in only one patient. Twelve (33%) of the 36 patients reported adverse effects: gastrointestinal symptoms in 8, CNS symptoms in 3, and others in 1. The antitumor efficacy of TAC-278 was insufficient while incidence of adverse effects was similar to other 5-FU derivatives in man and the clinical usefulness of the drug was hardly found. TAC-278 has been developed with an aim to give higher plasma concentrations of 5-FU in man. Even at a dose causing adverse effects, however, the clinical efficacy of TAC-278 was unsatisfactory. The study is a meaning tal eince the results suggest that there might be a more important factor than blood concentration of 5-FU to enhance an antitumor effect of 5-FU derivatives.

Adult↗
PubMed1981

Genetic complementation groups in cockayne syndrome.

Skin fibroblasts from patients with cockayne syndrome (CS cell) exhibited marked ultraviolet (UV) sensitivity as measured by colony-forming ability. Further, recovery of semiconservative DNA synthesis following UV irradiation was absent in CS cells, as it is in xeroderma pigmentosum cells. We found that the rate of semiconservative DNA synthesis measured at 12 h after 12 J/m2 of UV irradiation had recovered to nearly normal levels in binuclear cells obtained by the fusion of CS strains CS3BE (GM 1856) and CS7SE (GM1428) and of CS3BE (GM1856) and CS1BE (GM1629), but not of C57SE (GM1428) and CS1BE (GM1629). These results indicate that there are at least two genetic complementation groups in CS.

Cell Line↗
PubMed1975

Excision-repair of 4-nitroquinolin-1-oxide damage responsible for killing, mutation, and cancer.

Excision-repair of DNA base damage produced by 4-nitroquinoline-1-oxide (4NQO) was compared in Escherichia coli, human cells, and mouse cells. Paper chromotography of acid hydrolysates of DNA extracted from cells treated with 3H-labeled 4NQO revealed four peaks; two kinds of 4NQO-guanine adduct, one kind of 4NQO-adenine adduct, and free 4-aminoquinoline-1-oxide (4AQO). About 80% of the initially formed 4NQO-purine adducts were excised from DNA in E. coli uvrA+ cells during 60 min postincubation, but not at all in uvrA- (excisionless for uv damage) cells. Normal human cells excised about 60% of 4NQO-purine adducts during 24 hr postincubation, but xeroderma pigmentosum (excisionless) cells did not. A mouse cell line susceptible to repair of 4NQO-induced pretransformational damage also showed excision-repair ability for the 4NQO adducts. From these and other results, we conclude that the 4NQO-purine adducts and unstable 4NQO-guanine products (which release 4AQO) are, like pyrimidine dimers, repairable by excision-repair universal among E. coli, mouse, and human being, and that unexcised ones are probably the major cause of killing, mutation, and cancer.

4-Nitroquinoline-1-oxide↗