Experimental hypothyroidism increases apoptosis in dimethylbenzanthracene-induced mammary tumors.

LOPEZ-FONTANA CM; MASELLI, ME; SASSO CV; SANTIANO FE; SEMINO SN; CUELLO CARRION FD; JAHN GA; CARON RW

ONCOLOGY REPORTS

SPANDIDOS PUBL LTD

Lugar: Atenas; Año: 2013 vol. 30 p. 1651 - 1660

1021-335X

Epidemiological and in vitro data have not provided conclusive evidence concerning the involvement of thyroid hormones (THs) on mammary carcinogenesis. We used an in vivo model to assess the relationship between THs, adipose tissue and breast cancer development. Female Sprague‑Dawley rats were treated with a dose of 7,12-dimethylbenz(a)anthracene (15 mg/rat) at 55 days of age and were then divided into four experimental groups: hypothyroid rats (HypoT, 0.01% 6-N-propyl-2-thiouracil in drinking water), untreated control (EUT); hyperthyroid rats (HyperT, 0.25 mg/kg/day T4 s.c.) and vehicle-treated control rats. The latency of tumor appearance and the incidence and progression of tumors were determined. At sacrifice, blood samples were collected for hormone determinations and samples of tumor and mammary glands were obtained for immunohistological studies. HypoT rats had retarded growth and an increase in mammary fat. The latency was longer (p