Abstract
Summary
Intact and ovariectomized Sprague-Dawley rats with ME lesions placed prior to treatment with DMBA, showed a 30 and 0% mammary tumor incidence, respectively, in contrast to a 95 and 54% mammary tumor incidence in the respective nonlesioned control groups. Intact and ovariectomized rats lesioned 75 days after DMBA treatment showed a 120 and 80% increase, respectively, in number of palpable mammary tumors 10 days after treatment. In contrast the non-lesioned intact and ovariectomized control groups showed a 19% increase and a 27% decrease in number of palpable mammary tumors, respectively. After 25 days, stimulation of mammary tumor growth was still marked in the intact-lesioned group but regression occurred in the ovariectomized-lesioned group. These results indicate that ME lesions placed before DMBA treatment inhibit mammary tumorigenesis, presumably by increasing prolactin secretion and stimulating mammary growth, thereby leaving the mammary glands refractory to DMBA; ME lesions placed 75 days after DMBA treatment are believed to promote growth and development of mammary tumors by increasing prolactin secretion.
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