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    Tamoxifen research chemicals


    After surgery to remove early-stage breast cancer, many women are treated with a combination of chemotherapy medicines. If a woman is postmenopausal and the cancer is hormone-receptor-positive, she'll also take hormonal therapy (tamoxifen or an aromatase inhibitor) for 5 years. Treatments given after surgery are called adjuvant therapies and are given to lower the risk of the cancer coming back (recurrence). Results from studies presented at the 2009 San Antonio Breast Cancer Symposium continued to show the benefits of adjuvant treatments. One study showed that postmenopausal women diagnosed with early-stage, hormone-receptor-positive breast cancer that had spread to the lymph nodes who got adjuvant chemotherapy AND adjuvant hormonal therapy had a lower risk of recurrence and were more likely to be alive than women who got only hormonal therapy. The study also showed that starting hormonal therapy after chemotherapy was done was better than giving hormonal therapy and chemotherapy at the same time. A second study showed that a type of genetic test, called a genomic assay, can help figure out if women diagnosed with early-stage, hormone-receptor-positive breast cancer that has spread to the lymph nodes will benefit from adjuvant chemotherapy. purchase viagra online canada After surgery, women diagnosed with hormone-receptor-positive breast cancer usually take hormonal therapy medicine to reduce the risk of the cancer coming back (recurrence). Hormonal therapy medicines work in two ways: Doctors call treatment given after surgery adjuvant treatment. There are several types of hormonal therapy medicines. Tamoxifen, a selective estrogen receptor modulator (SERM), is one of the most well-known. Tamoxifen can be used to treat both premenopausal and postmenopausal women. The aromatase inhibitors: have been shown to be more effective at reducing recurrence risk in postmenopausal women and are now used more often than tamoxifen to treat women who’ve gone through menopause. Aromatase inhibitors aren’t used to reduce recurrence risk in premenopausal women.

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    Tamoxifen is a selective estrogen response modifier (SERM), protein kinase C inhibitor and anti-angiogenetic factor. Tamoxifen is a prodrug that is metabolized to active metabolites 4-hydroxytamoxifen (4-OHT) and endoxifen by cytochrome P450 isoforms CYP2D6 and CYP3A4. In breast cancer, the gene repressor activity of tamoxifen against ERBB2 is dependent upon PAX2. Blocks estradiol-stimulated VEGF production in breast tumor cells. Protein kinase C inhibitor. Induces apoptosis in human malignant glioma cell lines. Tamoxifen and its metabolite 4-hydroxytamoxifen are selective estrogen response modifiers (SERMs) that act as estrogen antagonists in mammary gland. Blocks estradiol-stimulated VEGF production in breast tumor cells. Resistance to tamoxifen therapy in some estrogen receptor positive breast cancers may originate from in utero exposure to endocrine disrupting chemicals, research in animal studies suggests. This study provides a new path forward in human research as about half of the breast cancers treated with this common cancer therapy do not respond well, say researchers. An animal study suggests that resistance to tamoxifen therapy in some estrogen receptor positive breast cancers may originate from in utero exposure to endocrine disrupting chemicals. The study provides a new path forward in human research as about half of the breast cancers treated with this common cancer therapy do not respond well, say researchers at the Georgetown Lombardi Comprehensive Cancer Center, who led the multi-institutional research. ), identified four genes that are linked to tamoxifen resistance and poor prognosis of breast cancer, by comparing results obtained in a new animal model, in human breast cancer cells grown in culture, and in publically available datasets collected from thousands of estrogen receptor positive breast cancer patients treated with tamoxifen. "Higher estrogen levels in utero have been known to increase risk of estrogen positive breast cancer in laboratory animals -- and humans -- but it wasn't known until this study that these elevated levels may also be responsible for tamoxifen resistance," says the study's co-lead author, Leena Hilakivi-Clarke, Ph D, a professor of oncology at Georgetown Lombardi.. Researchers further demonstrated that changes in these genes were reversed by adding well-tolerated epigenetic modifying drugs, valproic acid and hydralazine, to tamoxifen therapy regimen.

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