Abstract:Raloxifene and tamoxifen had similar effects on these mouse models of tamoxifen-naive and tamoxifen-resistant breast and endometrial cancer. Treatment with raloxifene following 5 years of adjuvant tamoxifen may not further decrease breast cancer recurrence and may increase endometrial cancer incidence.
“…In this study [19], athymic, ovariectomized mice were bitransplanted with tumors derived from human breast and endometrial cancer cells, some of which were tamoxifen naı¨ve and some of which had been exposed to tamoxifen for 6 months or ‡5 years. Tamoxifen was better than raloxifene at blocking the effects of low-dose estrogen on breast and endometrial cells not previously exposed to tamoxifen.…”
In this setting, raloxifene use among women with a history of breast cancer is related to stage at diagnosis and bone mineral density and is rare among women who have completed a 5-year course of adjuvant tamoxifen.
“…In this study [19], athymic, ovariectomized mice were bitransplanted with tumors derived from human breast and endometrial cancer cells, some of which were tamoxifen naı¨ve and some of which had been exposed to tamoxifen for 6 months or ‡5 years. Tamoxifen was better than raloxifene at blocking the effects of low-dose estrogen on breast and endometrial cells not previously exposed to tamoxifen.…”
In this setting, raloxifene use among women with a history of breast cancer is related to stage at diagnosis and bone mineral density and is rare among women who have completed a 5-year course of adjuvant tamoxifen.
“…The formula for a successful outcome in my quest to contribute, depended on two principal factors: a willingness to learn new laboratory techniques using relevant animal models that turned out to have significance for translational research in therapeutics and the willingness of innovative and committed individuals in industry and Yorkshire Cancer Research to invest in a young investigator [27]. This was followed by the generosity of a philanthropic organization, the Lynn Sage Breast Cancer Foundation in Chicago, who raised a million dollars a year for a decade for my tamoxifen team to define and understand the new science oestrogeninduced apoptosis [61][62][63][64][65][66][67].…”
“…Acquired resistance to SERMs is unique as the tumors are SERM stimulated for growth (Howell et al 1992). The first laboratory model (Gottardis and Jordan 1988;Gottardis et al 1990) of transplantable tamoxifen resistant cells demonstrated that 1) tamoxifen or estrogen can cause tumors to grow, 2) tumors require a liganded receptor to grow, 3) an aromatase inhibitors (estrogen deprivation) or a pure antiestrogen that causes ER degradation would be useful second line agents, 4) there was cross resistance with other SERMs (O'Regan et al 2002). Currently, numerous model systems exist to study SERM resistance.…”
Section: Evolution Of Serm Resistance As Deciphered By the Laboratorymentioning
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