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发布于:2020-11-27 13:16:59  访问:0 次 回复:0 篇
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Neuroscience Ku
The xenograft model is similar to the postmenopausal breast cancer patient in several respects.Aromatase is expressed in nonovarian tissue and is not regulated by gonadotropins.Although circulating levels of estrogen are low in postmenopausal women, the concentrations of estrogen in the breast are similar to premenopausal levels, in part, because of steroid buy Anthraquinone uptake and, in part, because of local synthesis via aromatase expressed in stromal cells, tumor epithelial cells, and adipocytes. Although expression of aromatase is limited to the tumor cells in the xenograft model and estrogen concentrations may be relatively high compared with patients, systemic aromatase inhibitor treatment will inhibit estrogen synthesis in all sites and reduce the amount taken up as well as that produced locally.An advantage of this xenograft model is that because tumor cells are ER positive and express aromatase, both antiestrogens and aromatase inhibitors can be studied.Although androstenedione is provided as a supplement because the adrenal hormones are deficient in the nude mice. Estrogens exert their proliferative effect on hormonedependent breast cancer cells by stimulating cell cycle progression.Studies have been shown that antiestrogen treatment or estrogen deprivation prevents MCF cells entering into S phase of the cell cycle. Preventing entry into S phase subsequently led to a decrease in the percentage of cells in S and M phase.Tumor growth rate is dependent on both proliferation rate and apoptotic rate.In addition to inducing cell cycle progression, estrogens are known to protect against cell death by apoptosis.Our results indicate that aromatase inhibitors have higher efficiency in inducing apoptosis than antiestrogens and EW.It is possible that the differences in efficacies of the three aromatase inhibitors resulted from differences in their abilities to inhibit aromatase activity.Whether it reflects other actions of the compound is unknown and will require additional investigation.APOPTOSIS SIGNALING PATHWAYS AND AROMATASE INHIBITORS to two estrogen response elements located within the bcl coding region. Collectively, downregulation of an antiapoptotic protein together with upregulation of a proapoptotic protein would be expected to produce a more powerful response and a greater induction of apoptosis.Activated purchase Anthraquinone caspase then initiates a cascade activation of downstream caspases, and. Caspase is believed to be the major executioner caspase downstream of caspase.Initiator caspases such as caspase or caspase can activate the apoptotic pathway not only by activating caspase but also through activation of caspase. Moreover, in vitro studies have shown that caspase and caspase have very similar substrate specificity, one of which is PARP. Additionally, levels of the activecleaved form of caspase were correlated with levels of PARP cleavage and an increased in apoptotic index.Activation of caspase and caspase and the inactivation of PARP correlated with a reduction in expression of the proforms of these enzymes.These results suggested that the activation of caspases observed in our studies is likely to be regulated at the protein level rather than at the transcription level.As a transcription factor, p increases transcription expression of several genes, including p and bax. Increased cmyc transcription and protein levels are an early response to treatment with E.E activates cmyc expression via the interaction of the EER complex with a bp estrogen response element in the cmyc promoter.
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