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M Koszalka

Publications and source records attributed to M Koszalka.

5 recordsLinked to original sources
PubMed1991

Comparative study of the influence of pregnancy and hormonal treatment on mammary carcinogenesis.

Since it has been shown that pregnancy protects the mammary gland from chemically induced carcinogenesis, this study was designed with the dual purpose of determining whether treatment of young virgin rats with the placental hormone chorionic gonadotropin (hCG) mimics pregnancy-induced changes in the tumourigenic response of the mammary gland and also whether the effect induced by both pregnancy and hormonal treatments was transitory, or a more permanent one, exerting the same effect when the period of time between delivery or termination of treatment and exposure to the carcinogen is lengthened. Virgin Sprague-Dawley rats were utilised in two experimental protocols. For protocol I, 50 day-old rats were either mated (Group II), or started receiving a daily intraperitoneal injection of 100 IU hCG (Group III) at age 50. Age-matched untreated virgin rats were used as controls (Group I). Twenty-one days after either delivery or termination of treatment all the animals received an intragastric dose of 8 mg DMBA/100 gbw. For the second protocol, 50 day-old virgin rats were also mated (Group V) or were treated with hCG for 21 days (Group VI); the resting period between delivery or termination of treatment was lengthened to 63 days, at which time they received a dose of DMBA. Age-matched controls (Group IV) received DMBA only. Tumourigenesis was evaluated 24 weeks post-carcinogen administration in all the groups. Pregnancy and hCG followed by the 21-day resting period significantly depressed mammary carcinogenesis to 11% and 6% respectively, compared with 63% in control animals. When the resting period was prolonged to 63 days there was also a significant depression in adenocarcinoma incidence to 9% in pregnancy (Group IV) in which it was observed that tumour incidence was also reduced as a consequence of aging at the time of exposure to the carcinogen. These results clearly indicate that hCG is as efficient as pregnancy and significantly reduces mammary carcinogenesis, and that the protective effect of both pregnancy and hCG treatment is long-lasting and both are more efficient than aging in reducing mammary carcinogenesis.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1990

Human chorionic gonadotropin and rat mammary cancer prevention.

The observation that mammary cancer induced by 7,12-dimethylbenz[a]anthracene (DMBA) in young, virgin, Sprague-Dawley rats is abolished by pregnancy led us to test the possibility of protecting the mammary gland from chemically induced carcinogenesis by using the placental hormone human chorionic gonadotropin (hCG). Fifty-day-old, outbred, virgin, Sprague-Dawley rats were utilized in two different experimental protocols. In protocol 1, four groups of virgin rats received either no hCG (group I) or a daily intraperitoneal injection of hCG at 1 IU (group II), 10 IU (group III), or 100 IU (group IV) for 21 days; group I and groups II-IV, at 21 days after the last injection, were given a single intragastric dose of 8 mg of DMBA per 100 g of body weight. In protocol 2, 50-day-old rats were treated with a single intragastric dose of 8 mg of DMBA per 100 g of body weight; 21 days later, they were separated into groups V and VI. Group V rats remained undisturbed, except for palpation twice a week for detection of tumor development. Group VI rats received a daily intraperitoneal injection of 100 IU of hCG for 60 days. Tumorigenesis was evaluated 24 and 30 weeks after carcinogen administration in animals in protocols 1 and 2, respectively. In protocol 1, in which animals (with the exception of the control group) were treated with hCG prior to carcinogen administration, the incidence of adenocarcinomas decreased in a dose-dependent manner, from 43.8% in the controls (group I) to 34.4%, 18.2%, and 6.15% in groups II-IV treated with 1, 10, or 100 IU of hCG, respectively. Among animals in protocol 2, hCG treatment significantly reduced the incidence of adenocarcinomas, from 100% in DMBA-treated rats (group V) to 45.5% in rats treated with DMBA plus hCG (group VI). These data indicate that hCG can prevent both initiation and progression of mammary carcinogenesis.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1990

Protective effect of chorionic gonadotropin on DMBA-induced mammary carcinogenesis.

The effect of the placental hormone chorionic gonadotropin (hCG) on 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary tumours was studied in young virgin Sprague-Dawley rats. This hormone when administered at a dose of 100 IU day-1 does not induce toxic effects, measured as alterations in body weight or weight of endocrine organs, and has a reversible effect on oestrous cycle. The lack of toxicity and the fact that hCG treatment terminated prior to administration of the chemical carcinogen DMBA protects the mammary gland from malignant transformation, led us to test the effect of hCG treatment on DMBA-initiated mammary tumours. Fifty day-old virgin Sprague-Dawley rats received intragastrically 8 mg DMBA per 100 g body weight and were divided into two groups: group I animals were treated with DMBA only and group II received DMBA at age 50 and in addition, a daily intraperitoneal injection of 100 IU hCG for days 21-81 post carcinogen administration. Tumorigenic response was evaluated by biweekly palpation of all animals and by complete autopsy 24 weeks after DMBA treatment. Group I animals developed an incidence of 100% of both tumours and adenocarcinomas. Group II animals developed a significantly lower incidence of tumours and adenocarcinomas, 51.5% and 45.5% respectively. In both groups lesions developed more frequently in thoracic than in abdominal mammary glands. It is postulated that hCG treatment, probably through stimulation of ovarian oestrogen and progesterone synthesis, induces differentiation of mammary epithelium that although affected by the carcinogen can still be rescued from malignant transformation.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1990

Effect of human chorionic gonadotropin on mammary gland differentiation and carcinogenesis.

The observation that mammary carcinogenesis is inhibited in rats which completed a pregnancy prior to exposure to the chemical carcinogen 7,12-dimethylbenz[a]anthracene (DMBA) led us to determine whether the protective effect of pregnancy could be mimicked by treatment with the placental hormone chorionic gonadotropin (hCG). We also studied the effect of this treatment on mammary gland structure and differentiation, and determined whether hCG exerts toxic or collateral effects on body weight and endocrine organs. The systemic effect of hCG on body wt and endocrine organs and mammary gland was studied in outbred virgin Sprague-Dawley rats which at the age of 50 days started receiving 100 IU hCG i.p. daily for 21 days. The animals were subdivided into nine groups of five animals each; one group was killed on the first day of and the others at 5, 10, 15 and 21 days of injection and 5, 10, 15 and 21 days post injection. The effect of the hormonal treatment on the estrous cycle was determined by studying the vaginal smears taken during and after the injection period. The following parameters were determined: body wt, weight and morphology of pituitary gland, adrenals, ovaries and uterine horns. Mammary glands were processed for histology, autoradiography for determination of DNA labeling index (DNA-LI) and whole mount preparation for morphometric studies. The effect of hCG on mammary carcinogenesis was studied in two groups of virgin rats; group I, which at the age of 50 days started receiving a daily i.p. injection of 100 IU hCG for 21 days; 21 days after the last injection they were given 8 mg DMBA/100 g body wt. Group II animals received DMBA only. hCG treated animals gained weight as a function of age at the same rate as controls. Treatment did not modify the weight of adrenal glands. The weight of ovaries, uterus and pituitary gland were transitorily increased by the 15th day of treatment, but had returned to the same values of controls by the time of DMBA administration. Treatment stimulated mammary gland differentiation, measured as a progressive reduction in number of terminal end buds and increase in the number of alveolar buds and lobules. The DNA-LI was significantly depressed in all terminal structures in the glands of treated animals. In group I animals hCG treatment decreased incidence of adenocarcinomas to 6.15 from 43.8% in group II animals.(ABSTRACT TRUNCATED AT 400 WORDS)

9,10-Dimethyl-1,2-benzanthracene↗