Biomedical subjects

C Sumi

Publications and source records attributed to C Sumi.

21 records · Page 2Linked to original sources

PubMed1980

Mammary carcinogenic effect of low-dose fission radiation in Wistar/Furth rats and its dependency on prolactin.

The mammary carcinogenic effect in rats of low-dose fission radiation and its dependency on prolactin were studied. A total of 141 female W/Fu rats were exposed to 4.8, 8.9, or 19.5 rads of fission radiation that had both fision neutrons of 2.0 million electron volts (MeV) and gamma ray components similar to those produced by the Hiroshima bomb. Only 1 of 48 rats (2.0%) developed mammary tumor (MT) after irradiation alone, whereas 20 of 48 rats (41.6%) developed MT's if prolactin was supplied shortly after irradiation by means of grafting of the prolactin-secreting pituitary tumor. Furthermore, MT's occurred in 11 of 45 rats (24.4%) treated with prolactin as late as 12 months after irradiation, which suggested the long-term survival of radiation-induced dormant MT cells. A correlation was found between the development of MT and the elevation of serum prolactin level; most MT's appeared shortly after the grafted mammotropic pituitary tumor became palpable. The growth of MT's appeared to be promoted by prolactin in collaboration with ovarian hormones; the growth of adenocarcinomas was dependent on prolactin and ovarian hormones, whereas the growth of fibroadenomas appeared to be less hormone-dependent. Much higher biologic effectiveness, especially in the low-dose range, was found with 2.0-MeV fission neutrons compared with 14.1-MeV fast neutrons or 180-kilovolt peak X-rays in rat mammary carcinogenesis.

Adenocarcinoma↗

PubMed1980

Synergism of diethylstilbestrol and other carcinogens in concurrent development of hepatic, mammary, and pituitary tumors in castrated male rats.

Castrated male WF rats, given implants of pellets containing 5.0 mg diethylstilbestrol (DES), were given N-butyl-N-nitrosourea (NBU) in small amounts, which alone produced no mammary tumors in intact female rats. Treatment resulted in the high yield of hepatic tumors (HT), mammary tumors (MT), and pituitary tumors (PT) concurrently in each rat. If animals were further treated with prolactin, the development of HT and MT was accelerated, whereas that of PT was suppressed. None of the intact or castrated rats receiving NBU and/or prolactin developed tumors in any tissues if DES treatment was omitted. Exposure of male rats, preconditioned similarly to NBU treatment, to 200 rads of 14.1-MeV fast-neutron radiation also elicited HT, MT, and PT with an efficiency comparable to that of NBU-treated rats. These findings indicate that DES played an essential role in the whole carcinogenic process in each tissue and that castrated male rats, if conditioned properly with estrogens, are useful for the study of the carcinogenesis mechanism in these tissues.

Animals↗

PubMedDate not supplied

Effects of sex steroid hormones on pancreatic cancer in the rat.

The incidence of spontaneous and induced neoplasms of the exocrine pancreas in rats is higher in males than in females. Castration, ovariectomy, and hormone replacement with estradiol and testosterone have been shown to influence the growth of carcinogen-induced preneoplastic foci in the azaserine-rat model of pancreatic carcinogenesis. Similar hormonal treatments have also influenced the growth of an azaserine-induced poorly differentiated acinar cell carcinoma that can be transplanted syngeneically in Lewis rats. The effect on growth of preneoplastic lesions and carcinomas is similar. The preneoplastic lesions and transplanted tumors grow faster in intact male rats than in castrated rats, and the growth of the lesions and tumors is inhibited by estrogen treatment. It appears that testosterone supports the growth of preneoplastic foci and carcinomas, whereas estrogen inhibits such growth. The mechanism is unknown and may be direct, or an indirect effect may be mediated through a peptide hormone. Tamoxifen treatment did not significantly influence the growth of the transplanted carcinomas in the rat model.

Animals↗