If the headaches persist beyond this point, and remain moderate or severe, preventive medicine should be instituted.
Background and Purpose--Because of their mixed estrogen-agonist and estrogen-antagonist properties, selective estrogen receptor modulators SERMs ; are considered promising substitutes for hormone replacement therapy. Raloxifen and other SERMs confer estrogen-like cardiovascular protective effects but lack the carcinogenic activity of exogenous estrogen. However, little is known about the cerebrovascular action of raloxifene. Therefore, we studied the effects of raloxifene on the mechanisms regulating rat cerebral artery tone. Methods and Results--Ring segments of the isolated rat posterior communicating cerebral arteries were mounted in a microvessel myograph for measurement of isometric tension. Whole-cell L-type voltage-sensitive Ca2 currents were recorded using the perforated patch-clamp technique. Raloxifwne 0.1 to 10 mol L ; reduced the contractile responses to U46619, phenylephrine, and endothelin-1 in normal Krebs solution or to CaCl2 in Ca2 -free, high K -containing solution. Raloxifene-induced relaxation was identical in endothelium-intact and endothelium-denuded rings. ICI 182780 had no effect on raloxifene-induced relaxation. Raloxiffne reduced L-type Ca2 currents with a pD2 of 5.98 0.06, close to that 6.44 0.09 ; for raloxifene-induced relaxation of 60 mmol L K -contracted rings. Conclusions--This study demonstrates that raloxifene acutely relaxes rat cerebral arteries largely via an endotheliumindependent mechanism, involving inhibition of Ca2 influx through L-type Ca2 channels. Stroke. 2004; 35: 000-000. ; Key Words: vasodilation cerebrovascular circulation rats.
Study of raloxifene and tamoxifen
As such initiatives grow, they are often supported by local government agencies and involve increased enforcement activities by local police services. At this stage of development, they frequently strongly resemble anti-drug market programmes initiated by the police or other state agencies, such as those considered in the next chapter which describes community policing approaches.
We're so passionate in our belief this is an extremely useful trial that will benefit women, " says Dr. Wolmark, who is also chairman of oncology at the Drexel University School of Medicine. "We think an injustice has been done to women by canceling the trial." In its appeal letter to NIH director Zerhouni, the NSABP said that the cancer institute's director was "acting unilaterally" and that the decision to cancel the trial "represents a dangerous and unjustified departure" from the agency's traditional review process. The appeal was "highly unusual" because the NSABP has a nearly 50-year relationship with the NCI, which is the primary source of its funding, says Kirsten Goldberg, editor and publisher of the Washington-based Cancer Letter, which tracks cancer research and funding. Drug firms typically provide free drugs or additional funding for NSABP trials. ; The NSABP has had a notable impact on breast-cancer treatment. For instance, the group's research led to the standard use of lumpectomy instead of radical mastectomy. And its STAR trial Study of Tamoxifen and Raloxifeen ; showed that the drugs can lower risk of breast cancer among high-risk women by 50% or more. That study led to a July FDA committee recommendation that raloxifene sold now as the bone drug Evista ; be approved for breastcancer prevention. The Stellar trial has been in the works since fall 2005, and had won approval from the NCI's division of cancer prevention and the agency's executive committee. But as the study was about to begin, Dr. Niederhuber stopped it, saying the agency wanted to review it further. In June, the NCI said it wouldn't fund the study after hearing reports from an expert panel convened by Dr. Niederhuber. The medical journal Lancet noted in a recent editorial that it was "troubling" that the NCI director stepped in to halt a trial that had been given "high marks" by seven NCI committees, including its top executive committee. "An independent investigation into how the decision was made and whether it was made fairly is warranted, " the Lancet wrote. The NCI declined to comment about the Lancet editorial. "Ultimately Dr. Niederhuber got the best scientific advice and acted on it, " said an NCI spokesman in an email. "He feels NCI now needs to move to a position of leadership in prevention for the next decade, utilizing genomics, whole-genome scans, rapid sequencing and sub-cellular imaging. The challenge is to accurately determine risk and match the many considerations about interventions with that risk. In other words, we need to find markers and match risk with the appropriate level of intervention. Patients are often not willing to trade healthy lives for side effects associated with interventions - unless they are convinced they know the risk." The National Breast Cancer Coalition says it supports the NCI's decision to focus on studies to develop better ways of predicting who is at risk for breast cancer. "We are very concerned about the approach of treating healthy women with drugs that are toxic in order to reduce the risk for very few who benefit, " says Carolina Hinestrosa, NBCC executive vice president.
Back to homepage celebrate with us about us • contact us • subscribe renew • advertise • classifieds • reprints issues health system edition drug topics daily news supplements web exclusives magazine subscribe renew drug topics e-alerts subscribe contact editorial contact sales classifieds reprints lists licensing events and meetings links to online resources medicare survival kit pharmacy facts and figures podcasts surveys drug information community pharmacy compounding government and law independent pharmacy managed care over-the-counter self-care special reports business and management clinical practice government and law professional practice technology allergies alzheimer's disease arthritis asthma cancer cardiovascular disease dermatology diabetes epilepsy gastroenterology infectious disease insomnia migraine multiple sclerosis obesity ophthalmology osteoporosis parkinson's disease respiratory sleep disorders substance abuse take ce listing of ces drug patent expirations medicare survival kit medication therapy management top 200 drugs all pharmacy facts + figures latebreakers medication errors new drug information new products drug topics daily news web exclusives study shows raloxifene may be acceptable for women coming off tamoxifen, say researchers jun 19, 2006 by: martin sipkoff drug topics dt capsules raloxifene, used to treat osteoporosis, may be just as effective in fighting breast cancer as tamoxifen.
Washington, dc: department of health and human services; december 200 dhhs niosh ; publication no 2005-10 jaapa: home in this issue past issues about us contact us subscribe to us advertise with us © 2007 haymarket media, inc and the american academy of physician assistants and efavirenz.
Raloxifene review
A dramatic decrease in the formation of R-4-G by UGT1A10 was observed with substrate concentrations of 25 M, suggesting substrate inhibition may be occurring Lin et al., 2001 ; . Therefore, Km and Vmax were calculated after truncation of the curve to exclude the inhibited rates and then overlaid onto the actual two-site binding curve fit for 1A10 Fig. 4 ; . Interestingly, 1A10 displayed complete selectivity for R-4-G formation, because R-6-G was not detected in these kinetic experiments. Raloxofene Glucuronidation by Human Liver and Intestinal Microsomes. Kinetic parameters for raloxifene glucuronidation were also determined from human liver and intestinal microsomes Table 2 ; . The Km and Vmax values for 6-glucuronidation in liver microsomes could not be determined due to limited substrate solubility. The average intrinsic clearance Vmax Km ; was highest for the 4 -glucuronide in jejunum microsomes, reaching 95 l min mg, which was approximately 6-fold greater than that observed for R-6-G formation 17 l min mg ; . In comparing liver and intestinal intrinsic clearance for R-4-glucuronidation, hepatic levels were found to be 3-fold lower. The rates of formation of R-6-G and R-4-G were then determined using a bank of 13 characterized human liver microsome samples. Based on previous experiments for the determination of Km for raloxifene glucuronidation, a saturating substrate concentration 200 M ; was used. As shown in Fig. 5A, the rate of R-6-G formation ranged from 0.43 to 1.6 nmol min mg 4-fold ; and for R-4-G, from 0.48 to 1.5 nmol min mg 3-fold ; . Furthermore, the rate of formation of R-6-G correlated strongly with UGT1A1-marker estradiol-3-glucuronidation Fisher et al., 2000 ; , exhibiting an r2 of 0.84 p 0.01 ; Fig. 5B ; . In contrast, the rate of R-4-G showed no correlation with 1A1 activity r2 0.13, p 0.05 ; . Finally, a weak correlation was observed between the rate of formation of R-6-G and R-4-G in human liver microsomes r2 0.36, p 0.03 ; . Effect of Alamethicin on Expressed UGTs, Human Liver, and Intestinal Microsomal Activity. To examine the effect of alamethicin on UGT activity, raloxifene was incubated with different expressed UGT forms, human liver, or intestinal microsomes in the presence or absence of alamethicin Fig. 6 ; . Regarding expressed UGT forms, the activity of expressed UGT1A9 and 1A10 was not increased significantly in the presence of alamethicin, whereas a more pronounced increase in activity was observed with UGT1A1 and 1A8. For example, the addition of alamethicin to UGT1A1 resulted in approximately a 40% increase in the amount R-6-G formed compared with control. In contrast, the addition of alamethicin to incubations of both pooled human liver and jejunum microsomes resulted in a significant increase in the rate of formation of both raloxifene glucuronides. An increase in activity from 0.11 to 0.85 nmol min mg 8-fold ; was observed for the formation of R-6-G in jejunum microsomes. Similarly, an increase from 0.44 to 3.8 nmol min mg 9-fold ; was observed for the formation of R-4-G in the same system. In liver microsomes, an increase from 0.36 to 1.4 nmol min mg 4-fold ; and an increase from 0.38 to 1.1 nmol min mg 3-fold ; were observed for the formation of R-6-G and R-4-G, respectively. Discussion The contribution of intestinal glucuronidation to the first-pass metabolism of orally ingested xenobiotics in humans has gained considerable interest in recent years Shen et al., 1997; Czernik et al., 2000 ; . Raloxifene represents a clear example of a drug that does not undergo significant P450-dependent oxidation Hochner-Celnikier, 1999 ; , but rather where glucuronidation is the major route of metabolism. The present studies used various in vitro systems to identify and characterize the UGT forms responsible for R-4-G and R-6-G formation and to differentiate the contribution of hepatic and intestinal tissues to.
STAR trial Study of Tamoxifen and Raloxifene ; were announced by the National Cancer Institute NCI ; , BCA's critical analysis and perspective were captured by major newspapers, including USA Today and the Chicago Tribune. The STAR trial studied the use of these two drugs in women who have not had breast cancer but who have a higher than average risk of getting the disease. While the results of the trial and many news reports talked about using the drugs in this setting as breast cancer "prevention, " we noted that the results were about risk reduction, not prevention. In our press release, e-alert, and newsletter, we urged caution in interpreting the trial results, pointing out that while the NCI claimed that raloxifene was shown to be a better drug for preventing breast cancer, very few differences were actually found between tamoxifen and raloxifene and sustiva.
Complete Phase II and III clinical evaluation of M for E and M for H based regimens Consider evaluation of other drug combinations e.g., high dose rifamycins and moxi combos If data are supportive: Registration of M for E and or M for H in 2011.
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Work with your doctor to learn all you can about your medicines and how to use them effectively and vaseretic.
Tamoxifen has agonist effects on uterine endothelium and is associated with an increased risk of endometrial cancer in adjuvant trials Breast Cancer Trialists Collaborative Group, 1998 ; . In contrast, raloxifene appears to have neutral actions on uterine endothelium and is not associated with an increased risk of endometrial cancer.
Summaries of complaints and rulings are posted quarterly by the Prescription Medicine Code of Practice Authority, which deals with all alleged breaches of the ABPI code. Data is available back to 1993 at and ethambutol.
Osteoporosis, osteoprotegerin, postmenopause, vertebra fracture, 540 osteopenia, echography, osteoporosis, 542 osteoporosis, bisphosphonic acid derivative, calcitonin, selective estrogen receptor modulator, 541 - bone mass, estradiol, osteoclast differentiation factor, osteoprotegerin, postmenopause, vertebra fracture, 540 - echography, osteopenia, 542 osteoprotegerin, bone mass, estradiol, osteoclast differentiation factor, osteoporosis, postmenopause, vertebra fracture, 540 outcomes research, artery perfusion, obstetrics, twin pregnancy, twin twin transfusion syndrome, 470 outpatient, hospital patient, labor induction, misoprostol, uterine cervix, 461 ovarian vein, vein thrombosis, 689 ovariectomy, cell maturation, conjugated estrogen, raloxifene, resveratrol, squamous cell, tibolone, vagina, 628 ovary, clomifene citrate, endometrium, histopathology, uterine cervix, 697 ovary cancer, breast cancer, 683 - cancer recurrence, 700 - cancer recurrence, prognosis, 699 - cancer staging, laparoscopy, peritoneum cancer, uterine tube disease, uterus cancer, 695 - cisplatin, 678 - cyclic AMP, G protein coupled receptor, inositol phosphate, sphingosylphosphorylcholine, 692 - cytochrome P450 isoenzyme, 686 - DNA repair, genetic polymorphism, 685 ovary carcinoma, breast carcinoma, hormonal carcinogenesis, sex hormone, uterus carcinoma, 679 - cancer grading, cell nucleus, 682 - colorectal carcinoma, lung carcinoma, prostate carcinoma, 659 - extrapulmonary tuberculosis, 496 ovary cyst, fetus echography, lymphangioma, torsion, 696 ovary disease, 681 ovary follicle cell, female infertility, human menopausal gonadotropin, intrauterine insemination, ovary hyperstimulation, 587 ovary follicle development, Muellerian inhibiting factor, ovary polycystic disease, 677 ovary hyperstimulation, female infertility, human menopausal gonadotropin, intrauterine insemination, ovary follicle cell, 587 ovary polycystic disease, endocrine disease, obesity, 680 - genetic polymorphism, plasminogen activator inhibitor 1, 698 - Muellerian inhibiting factor, ovary follicle development, 677 overactive bladder, cholinergic receptor blocking agent, detrusor dyssynergia, interstitial cystitis, 591 oxidative stress, biochemical marker, endothelium lesion, placenta circulation, preeclampsia, screening test, 453 oxidized low density lipoprotein, aryldialkylphosphatase, preeclampsia, pregnancy, 520 oxygen tension, gene expression regulation, hypoxia inducible factor 1alpha, 636 pain, interstitial cystitis, menstrual cycle, nociception, 545 Papanicolaou test, colon adenocarcinoma, uterine cervix carcinoma, 645 parasitemia, fetus disease, Human immunodeficiency virus infection, malaria falciparum, 494 paternity, adolescent pregnancy, 361 pathological anatomy, pelvic organ prolapse, pelvis, 605 patient attitude, patient satisfaction, vaginal delivery, 462 patient compliance, conjugated estrogen plus medroxyprogesterone acetate, hormonal therapy, menopausal syndrome, oral contraceptive agent, postmenopause, 558 patient satisfaction, patient attitude, vaginal delivery, 462 pelvic organ prolapse, 619 - abdominal surgery, 649 - collagen, xenograft, 603 - feces incontinence, urine incontinence, 606 - levator ani muscle, stress incontinence, 617 Section 10 vol 89.2.
Because raloxirene is associated with a decreased incidence of breast cancer in postmenopausal osteoporotic women, some patients may find it more acceptable than estrogen replacement therapy and myambutol.
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1. Genant HK, Lucas J, Weiss S, et al. Low-dose esterified estrogen therapy: effects on bone, plasma estradiol concentrations, endometrium, and lipid levels. Estratab Osteoporosis Study Group. Arch Intern Med. 1997; 157: 2609-2615. Lindsay R, Hart DM, Clark DM. The minimum effective dose of estrogen for prevention of postmenopausal bone loss. Obstet Gynecol. 1984; 63: 759-763. Ettinger B, Genant HK, Steiger P, Madvig P. Low-dosage micronized 17 beta-estradiol prevents bone loss in postmenopausal women. J Obstet Gynecol. 1992; 166: 479-488. Recker RR, Davies KM, Dowd RM, Heaney RP. The effect of low-dose continuous estrogen and progesterone therapy with calcium and vitamin D on bone in elderly women. A randomized, controlled trial. Ann Intern Med. 1999; 130: 897-904. Lindsay R, Gallagher JC, Kleerekoper M, Pickar JH. Effect of lower doses of conjugated equine estrogens with and without medroxyprogesterone acetate on bone in early postmenopausal women. JAMA. 2002; 287: 2668-2676. Prestwood KM, Kenny AM, Kleppinger A, Kulldorff M. Ultralow-dose micronized 17-estradiol and bone density and bone metabolism in older women: a randomized controlled trial. JAMA. 2003; 290: 1042-1048. Evans SF, Davie MW. Low and conventional dose transdermal oestradiol are equally effective at preventing bone loss in spine and femur at all postmenopausal ages. Clin Endocrinol Oxf ; . 1996; 44: 79-84. Delmas PD, Pornel B, Felsenberg D, et al. Three-year follow-up of the use of transdermal 17beta-estradiol matrix patches for the prevention of bone loss in early postmenopausal women. J Obstet Gynecol. 2001; 184: 32-40. Ettinger B, Grady D, Foegh M, Hanes V. Osteoporosis prevention with unopposed ultra-low-dose transdermal estradiol. Obstet Gynecol. In press. 10. Delmas PD, Ensrud KE, Adachi JD, et al; Multiple Outcomes of Raloxifene Evaluation Investigators. Efficacy of raloxiifene on vertebral fracture risk reduction in postmenopausal women with osteoporosis: four-year results from a randomized clinical trial. J Clin Endocrinol Metab. 2002; 87: 3609-3617. Black DM, Thompson DE, Bauer DC, et al. Fracture risk reduction with alendronate in women with osteoporosis: the Fracture Intervention Trial. FIT Research Group [published correction appears in J Clin Endocrinol Metab. 2001; 86: 938]. J Clin Endocrinol Metab. 2000; 85: 4118-4124.
Among the prevalent MBSP screeners, there was some consistency in the validity measures across the various ethnic groups Table 24 ; . Aboriginals and Asians had the lowest concordance 89.9% ; , sensitivity 78.4%, 81.0% ; , PPV 93.1%, 88.1% ; , and kappa 0.78, 0.77 ; . Asians also had the lowest specificity 94.4% ; and the Aboriginals also had the lowest NPV 88.5% ; . The French and Other Europeans had the highest concordance 93.3% ; , sensitivity 87.6%, 91.3% ; and kappa 0.86, 0.87 ; . The French also had the highest NPV 91.6% ; . The British and Northern Europeans had the highest PPV 96.3% ; , while the Southern Europeans had the highest specificity 98.0% ; . However, there were only few statistically significant differences. Other Europeans had statistically higher sensitivity than Aboriginals, while the French and British had a statistically higher PPV than the Asians. Table 24. Self-reported HRT use between screens in the MBSP compared to DPIN prescriptions, by ethnic background and etoposide.
Abbreviations: ALT SGPT alanine transaminase, AST SGOT aspartate transaminase, GGT gamma-glutamyl transferase, MCH mean corpuscular hemoglobin, MCHC mean corpuscular hemoglobin concentration, MCV mean corpuscular volume, PL RLX060 placebo up to month 12 and raaloxifene HCl 60 mg at months 12-24, PL RLX120 placebo up to month 12 and raloxifene HCl 120 mg at months 12-24, PTH parathyroid hormone, RBC red blood cell, UA urinalysis, WBC white blood cell. a Within-group change significantly different from baseline p 0.05 ; . b Between-group difference using analysis of variance.
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| Raloxifene side effectsDurect is focused on developing innovative drug-delivery technologies, especially in the area of pain medication. After a series of product development agreements in 2002 aimed at widening its drugdelivery product pipeline, Durect capped off the year with a development distribution and vepesid.
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Endometrium in postmenopausal women. N Engl J Med. 1997; 337: 1641-7. Ettinger B, Black DM, Mitlak BH, Knickerbocker RK, Nickelsen T, et al. Reduction of vertebral fracture risk in postmenopausal women with osteoporosis treated with raloxifene: results from a 3-year randomized clinical trial. Multiple Outcomes of Raloxifene Evaluation MORE ; Investigators. JAMA. 1999; 282: 637-45. Fisher B, Costantino JP, Wickerham DL, Redmond CK, Kavanah M, et al. Tamoxifen for prevention of breast cancer: report of the National Surgical Adjuvant Breast and Bowel Project P-1 Study. J Natl Cancer Inst. 1998; 90: 1371-88. Cummings SR, Eckert S, Krueger KA, Grady D, Powles TJ, et al. TThe effect of raloxifene on risk of breast cancer in postmenopausal women: results from the MORE randomized trial. Multiple Outcomes of Raloxifene Evaluation. JAMA. 1999; 281: 2189-97. McDonald CC, Alexander FE, Whyte BW, Forrest AP, Stewart HJ. Cardiac and vascular morbidity in women receiving adjuvant tamoxifen for breast cancer in a randomised trial. The Scottish Cancer Trials Breast Group. BMJ. 1995; 311: 977-80. BW, Kuller LH, Wild RA, Paul S, Farmer M, et al. Effects of raloxifene on serum lipids and coagulation factors in healthy postmenopausal women. JAMA. 1998; 279: 1445-51. Barrett-Connor E, Grady D, Sashegyi A, Anderson PW, Cox DA, et al. Raloxifene and cardiovascular events in osteoporotic postmenopausal women: four-year results from the MORE Multiple Outcomes of Raloxifene Evaluation ; randomized trial. JAMA. 2002; 287: 847-57. Yaffe K, Krueger K, Sarkar S, Grady D, Barrett-Connor E, et al. Cognitive function in postmenopausal women treated with raloxifene. N Engl J Med. 2001; 344: 1207-1213. McMeekin DS, Gordon A, Fowler J, Melemed A, Buller R, et al. A phase II trial of arzoxifene, a selective estrogen response modulator, in patients with recurrent or advanced endometrial cancer. Gynecol Oncol. 2003; 90: 64-9. Schiff R, Chamness GC, Brown PH. Advances in breast cancer treatment and prevention: preclinical studies on aromatase inhibitors and new selective estrogen receptor modulators SERMs ; . Breast Cancer Res. 2003; 5: 228-31 and famciclovir.
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Older. It is estimated that 12.5 % of women will have breast cancer during their lifetime. The study puts 87.5 % women who will nor develop breast cancer are subjected to the treatment with Tamoxifen and raloxifene. Every chemotherapy has adverse side effects in some people, therefore some of these women will have adverse effects only for the sake of treatment rather than preventing cancer. Thrust of the study is to show the difference in efficacy between Tamoxifen and raloxifene Novel saliva tests have following features: 1. Early diagnosis of cancer, based upon the concentration of proteonic cancer marker antigen PCM ; versus CT scan of the developed tumor. 2. Diagnosis of specific type of cancer is achieved by using respective anti sera versus current practice based upon the region organ of the tumor. 3. Test can be used to monitor the efficacy of chemotherapy, based upon the concentration of PCM before and after therapy, versus the current practice of determining the size of tumor 4. This test will eliminate unwarranted X-ray exposure and will replace or reduce the practice of CT scan. 5. The test will never be falsely negative, because, we all carry genes for cancer and at any given time mutated cells are bound to be present so also PCMs. It is the concentration of PCM that determines the pre or early cancerous state. Currently, the set cut off level is 1: 1000 for ELISA titer 100 l for positive test. 6. Non-invasively collected saliva is used in place of currently practiced blood serum to assay PCMs. 7. The use of saliva permits simple ELISA versus complicated double sandwich ELISA if serum is used. 8. The test for early diagnosis of cancer should be performed on yearly basis. Individuals showing ELISA titer 100 l, 1: 1000 or more against the mixture of PCMs antibodies, should be assayed for individual PCM to diagnose the specific type of cancer. 9. An early diagnosis of cancer will revolutionize the cancer field. No body will have to wait until the CT scan recognizes tumor. For more information please contact: Binie V. Lipps, Ph. D., President, Ophidia Products, Inc. 11320 South Post Oak, Suite 203 Houston, Texas 77035 Tel: 713 723-6845 E-mail: bvl ophidia.
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Consider raloxifene, a selective oestrogen-receptor modulator, for postmenopausal women with established osteoporosis who are unable to take bisphosphonates and or are at high risk of breast cancer. Raloxifene reduces the risk of vertebral fractures but, similar to etidronate and ibandronic acid, it has not shown an effect on non-vertebral fractures22, 23, and thus is less suitable for women at high risk of hip fracture. In postmenopausal women with osteoporosis and a previous fracture, raloxifene reduced the relative risk of a radiographically detected vertebral fracture by about 30% over 3 years absolute risk over 3 years was 14.7% with raloxifene vs 21.2% with placebo, NNT 15 ; .23 The added advantage of raloxifene is that it may protect against breast cancer. Over 8 years, raloxifene reduced the relative hazard of invasive oestrogen receptorpositive breast cancer by 76% 0.8 cases per 1000 womanyears with raloxifene vs 3.2 cases per 1000 womanyears with placebo ; .24 The advantages of fracture and breast cancer risk reduction with raloxifene need to be weighed against the increased risk of thromboembolic disorders for individual women. Raloxifene is associated with a 3-fold increased risk of venous thromboembolism.23 In a study of the effect of raloxifene on breast cancer and coronary events, the absolute risk reduction over 5.6 years for invasive breast cancer with raloxifene 1.2 per 1000 womanyears ; was largely offset by an increased absolute risk of venous thromboembolism 1.2 per 1000 womanyears ; and fatal stroke 0.7 per 1000 womanyears ; compared with placebo.25 Raloxifene is contraindicated in women at high risk of venous thromboembolism, such as those who are immobilised for long periods. Other side effects such as hot flushes and leg cramps are common and could offset the benefits in some women.23.
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Abstract. The impact of 17-estradiol and antiestrogens on uterine cancer cells is poorly understood. The aim of this study was to determine the impact of 17-estradiol, 4-hydroxytamoxifen, raloxifene and ICI 182 780 on the cell proliferation of six uterine cancer cell lines: HeLa, HEC-1-A, KLE, RL95-2, Ishikawa and EN-1078D. The effects of these compounds on the cell proliferation of the six uterine cancer cell lines were studied in the presence and absence of estrogens phenol red and serum deprivation of sex steroids ; . In a general manner, 17-estradiol and 4-hydroxytamoxifen showed similarities in their effects whereas raloxifene showed a different pattern of cell proliferation agonistic and antagonistic ; and ICI 182 780 had antagonistic activity. In the presence and absence of estrogens, we observed that each cell line had diverse expression of ER, ER, GPR30 and REA. GPR30 mRNA expression was significantly reduced in a serum phenol-free medium. REA mRNA expression was not influenced by the media. Results demonstrated the importance of removing phenol red and the use of deprived serum when studying uterine cancer cells in relationship with 17-estradiol and antiestrogens. The affinity of each compound to the binding of ER and ER was very similar with the exception of raloxifene that had a preference for ER binding. Akt phosphorylation activity was reduced in cells cultured in a phenol red- and steroid-free culture medium indicating that the presence of steroids in the culture media can influence the activity of this survival pathway. Our results suggest that the expression of ER, ER and GPR30 are influenced by sex steroids and might play a role in the response of cells to 17estradiol and antiestrogens but are not the only factors involved in this process.
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That COX2-selective inhibitors are members of the NSAID class and all produce their therapeutic effects through the common mechanism of inhibiting COX2; so maybe these newer drugs should more accurately be termed `COX1-sparing' than COX2-selective40. The potential for drugs to produce both therapeutic and deleterious effects is dependent not on their name but on their biological effects TABLE 1, for instance, raloxifene gyno.
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