Our stretches of the Blackwater are as follows: Upstream of the car park at Station Road Wickham Bishops (through the farm gate on the other side of the road) upstream for about 1/4 mile, passing under the trestle bridge and as far as the golf course (there is a small pool at the point where our stretch ends). Downstream from the car park, again about 1/4 mile, to the double bend at the end of the meadow. The Wickham Hall stretch starts here, but access to it from the meadow is blocked(ish), so most anglers will access the stretch from the Wickham Hall car park. From the Wickham Hall car park (signposted), walk down the track to the river. IMPORTANT – for the 2011/12 season onwards our access route has been revised, please refer to the following Wickham Hall Farm River Revised Access Map. You are roughly in the middle of the stretch when you arrive at the river. Upstream it extends for about 3/4 mile to meet the stretch above. Two kinds of surgery can be performed to reduce the risk of breast cancer in a woman who has never been diagnosed with breast cancer but is known to be at very high risk of the disease. A woman can be at very high risk of developing breast cancer if she has a strong family history of breast and/or ovarian cancer, a deleterious (disease-causing) mutation in the BRCA1 gene or the BRCA2 gene, or a high-penetrance mutation in one of several other genes associated with breast cancer risk, such as TP53 or PTEN. The most common risk-reducing surgery is bilateral prophylactic mastectomy (also called bilateral risk-reducing mastectomy). Bilateral prophylactic mastectomy may involve complete removal of both breasts, including the nipples (total mastectomy), or it may involve removal of as much breast tissue as possible while leaving the nipples intact (subcutaneous or nipple-sparing mastectomy). Subcutaneous mastectomies preserve the nipple and allow for more natural-looking breasts if a woman chooses to have breast reconstruction surgery afterward. However, total mastectomy provides the greatest breast cancer risk reduction because more breast tissue is removed in this procedure than in a subcutaneous mastectomy (1). Even with total mastectomy, not all breast tissue that may be at risk of becoming cancerous in the future can be removed.
Besides female sex, advancing age is the biggest risk factor for breast cancer. Reproductive factors that increase exposure to endogenous estrogen, such as early menarche and late menopause, increase risk, as does the use of combination estrogen-progesterone hormones after menopause. Nulliparity and alcohol consumption also are associated with increased risk. Women with a family history or personal history of invasive breast cancer, ductal carcinoma , or a history of breast biopsies that show benign proliferative disease have an increased risk of breast cancer.[1-4] Increased breast density is associated with increased risk. It is often a heritable trait but is also seen more frequently in nulliparous women, women whose first pregnancy occurs late in life, and women who use postmenopausal hormones and alcohol. Exposure to ionizing radiation, especially during puberty or young adulthood, and the inheritance of detrimental genetic mutations increase breast cancer risk. Note: Separate PDQ summaries on Breast Cancer Screening; Breast Cancer Treatment; Male Breast Cancer Treatment; Breast Cancer Treatment During Pregnancy; and Levels of Evidence for Cancer Screening and Prevention Studies are also available. Afimoxifene, also known as 4-hydroxytamoxifen (4-OHT, 4-HT, OHTAM, others), is a selective estrogen receptor modulator (SERM) of the triphenylethylene group and the major active metabolite of tamoxifen. A study in France on 55 women showed that rubbing afimoxifene on the skin was as effective as oral tamoxifen at slowing breast cancer growth. A United States trial will compare 6 weeks use before breast cancer surgery. Skin application can reduce systemic levels by a factor of nine and this is expected to reduce the unpleasant side-effects of tamoxifen.
The link between hormones and breast cancer growth and development has been recognized for more than a century. Estrogen stimulates the proliferation of breast epithelial cells, and both endogenous and exogenous estrogens have been implicated in the pathogenesis of breast cancer. Classically, estrogen action at target sites around the body is mediated through related but distinct estrogen receptors (ERs), designated ERα and ERβ, to alter gene expression. This accumulating understanding of the mechanism of action of estrogen led ultimately to the design of antiestrogenic agents that work by virtue of their interaction with the ER; these drugs have come to be known as selective estrogen receptor modulators (SERMs). Tamoxifen, a SERM, emerged as the first antiestrogenic agent that is clinically applicable to breast cancer. Tamoxifen became the “gold standard” and established the principles of tumor targeting and identified the appropriate treatment strategy to aid survivorship in breast cancer patients, with enhancement of disease-free survival and a 50% decrease in recurrences observed in ER-positive patients 15 years after diagnosis. However, because of the many adverse events in the use of tamoxifen, some of which have contributed to significant morbidity and mortality, drug modification which has resulted in fewer incidences of adverse events without compromising the therapeutic effect for breast cancer prevention may face an easier road to acceptance. In patients with early-stage breast cancer, 5 years of treatment with the selective estrogen receptor modulator (SERM) tamoxifen reduces breast cancer recurrence and mortality, whereas more than 5 years of tamoxifen does not further reduce breast cancer recurrence and doubles the risk of endometrial cancer. We evaluated the effects on tumor growth of raloxifene, another SERM, after tamoxifen treatment in mouse models of breast and endometrial cancers. Athymic, ovariectomized mice were bitransplanted with tumors derived from human breast cancer and endometrial cancer cells that either were tamoxifen-naive or had been exposed to tamoxifen for short (6 months) or long ( = .001) tumors. Raloxifene and tamoxifen had similar inhibitory effects on the growth of short-term tamoxifen-exposed breast tumors. Raloxifene and tamoxifen had similar stimulatory effects on the growth of breast and endometrial tumors that had been exposed to at least 5 years of tamoxifen. However, neither drug blocked the stimulatory effects of estrogen on the growth of these tumors. Raloxifene was less effective than tamoxifen ( Raloxifene and tamoxifen had similar effects on these mouse models of tamoxifen-naive and tamoxifen-resistant breast and endometrial cancer.
Jun 1, 1999. The unusual target site-specific action as an estrogen or as an antiestrogen was true for both tamoxifen and raloxifene 29, 30. Lacassagne's. Kosher Pharmaceuticals is an ISO 9008 certified company. We export prescription and over-the-counter OTC pharmaceuticals, nutritional products, active pharmaceutical ingredients API and veterinary medicines.