HYPERTHYROIDISM DECREASES MAMMARY CARCINOGENESIS IN RATS: ROLE OF THE OVARIAN STEROIDS

ZYLA LEILA; SASSO CORINA VERÓNICA; SANTIANO FLAVIA; PISTONE CREYDT VIRGINIA; LÓPEZ FONTANA CONSTANZA; CARÓN RUBÉN

Estancia Grande, San Luis

Congreso; XXXII Reunión Científica Anual de la Sociedad de Biología de Cuyo; 2014

We aim to assess whether changes in ovarian hormonal status affect participation of thyroid hormones on the development of mammary cancer (CaM). Female Sprague-Dawley rats were treated per os with a single dose of DMBA (15mg/rat) at 55 days of age and divided into euthyroid (EUT, n=28) and hyperthyroid rats (HYPER, 0.25mg/kg/day T4 s.c , n=32). On day 30, rats of both groups were ovariectomized (OVX) or sham operated (SHAM). All the animals were weighted weekly and observed until the appearance of the first palpable tumor. The latency, incidence and progression of tumors were determined. At sacrifice, whole blood samples and a piece of normal mammary gland and tumor were taken for hormone determinations and histological analyses. Statistical analysis was performed by ANOVA I and Chi square (IC>95%). OVX decreased the incidence and increased survival regardless the thyroid status. The absence of estrogen in HYPER completely abolished CaM incidence. The latency and the tumor growth rate were similar in HYPER SHAM, EUT SHAM and EUT OVX. However, tumors of SHAM rats were of a more aggressive histological type than OVX. No statistical differences were observed in GH and prolactin levels. In conclusion, hyperthyroidism decreased mammary carcinogenesis and enhanced the protective effect of OVX. The presence of estrogen, regardless of thyroid status, induced tumors with more aggressive behavior.