Breast Serum
«Triactol Breast Enlargement Cream | Increase Breast Size In 4 Weeks
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ScarAway Professional Grade Silicone Scar Treatment Sheets – Full Dr. Recommended 12 Week Supply 12 Multi-Use Patches with Free Storage Case Included $28.99 ScarAwayTM helps restore raised and discolored scars to a more natural color and texture, using the same technology trusted by burn centers and plastic surgeons. Using ScarAway on newly healed wounds helps prevent the formation of unsightly scars. Even scars that are years old from burns, surgical procedures and injuries show significant improvement with ScarAway. Previously available only to medi… |
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Breast Enhancement Cream $31.00 Enlarge your breasts naturally and fast. Natureday Breast Enhancement Cream (4 Oz) consists of a proprietary blend of mastogenic herbs and exotic plant extracts that have been proven to increase breast size by stimulating new cell growth in the mammary glands (breast tissue)…. |
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Brand New Booty. Female Butt Enlargement Enhancement and Body Support 3.0 Matrix Capsules $54.95 It almost seems unfair. Some women have that shapely hourglass figure that turns heads. But how can you achieve the same sexy figure? By using our natural booty enhancement complex that’s how! This is a quick and easy solution that may help in creating a round, apple bottom figure with full buttocks. Finally, a simple solution that requires no shots, injections or other risky surgical procedures…. |
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NeoGenomics and Power3 to commercialize blood serum-based tests for the early detection of breast cancer and other diseases.: An article from: BIOTECH Patent News $9.95 This digital document is an article from BIOTECH Patent News, published by Thomson Gale on April 1, 2007. The length of the article is 1052 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.Citation DetailsTitle: NeoGenomi… |
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Establishing a Method for Measuring Serum Methylmalonic Acid and Application to Women with a History of Breast Cancer $25.95 This is a AIR FORCE INST OF TECH WRIGHT-PATTERSONAFB OH report procured by the Pentagon and made available for public release. It has been reproduced in the best form available to the Pentagon. It is not spiral-bound, but rather assembled with Velobinding in a soft, white linen cover. The Storming Media report number is A941704. The abstract provided by the Pentagon follows: Serum concentrations o… |
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Watch for hypernatremic breast-feeding problems: timing of first visit, coding questions: jaundice, low weight: check serum sodium.: An article from: Pediatric News $5.95 This digital document is an article from Pediatric News, published by International Medical News Group on February 1, 2004. The length of the article is 1053 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.Citation Detai… |
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An integrated approach utilizing liquid separations, protein microarrays and tandem mass spectrometry towards understanding phosphorylation, glycosylation and humoral response changes in cancer. $49.99 The development and application of an integrated approach that utilizes liquid separations, protein microarrays and mass spectrometry with the goal of understanding breast, pancreatic and colon cancer progression is described. In order to understand breast cancer progression, two liquid separation techniques for the generation of protein microarrays from pre-malignant and malignant breast cancer cell lines which were subsequently probed for phosphoproteins was pursued. Out of 140 positively phosphorylated array spots, 85 were differentially phosphorylated. This corresponded to 75 unique proteins. 51 phosphorylation sites were identified by tandem MS/MS in 27 of these proteins. Phosphorylation changes were dominant in proteins involved in transcriptional and translational control as well as apoptosis and cytoskeletal regulation. A strategy for global glycoprotein profiling in serum and plasma was also developed. Glycoprotein microarrays of enriched and separated N-linked glycoproteins from serum and plasma from normal controls and patients with pancreatic cancer and colorectal cancer were generated. The specific sugar moieties on glycans were assessed using biotinylated lectins coupled with Alexa-flor conjugated streptavidin. In both cancers sialylation and fucosylation changes were dominant. Principal component analysis and hierarchical clustering analysis showed that this strategy successfully classified serum/plasma groups based on overall glycan expression profiles. The utility of protein microarrays for identifying potential markers of pancreatic cancer was also explored. Proteins from MIAPACA, a pancreatic cancer cell line, were fractionated in 2 dimensions and arrayed on nitrocellulose slides. The slides were hybridized with multiple serum samples from normal controls and patients diagnosed with pancreatic cancer in order to find specific cancer proteins that elicited an antigen-antibody response to the serum samples. Wilcoxon rank sum tests followed by the |
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An integrated approach utilizing liquid separations, protein microarrays and tandem mass spectrometry towards understanding phosphorylation, glycosylation and humoral response changes in cancer. $49.99 The development and application of an integrated approach that utilizes liquid separations, protein microarrays and mass spectrometry with the goal of understanding breast, pancreatic and colon cancer progression is described. In order to understand breast cancer progression, two liquid separation techniques for the generation of protein microarrays from pre-malignant and malignant breast cancer cell lines which were subsequently probed for phosphoproteins was pursued. Out of 140 positively phosphorylated array spots, 85 were differentially phosphorylated. This corresponded to 75 unique proteins. 51 phosphorylation sites were identified by tandem MS/MS in 27 of these proteins. Phosphorylation changes were dominant in proteins involved in transcriptional and translational control as well as apoptosis and cytoskeletal regulation. A strategy for global glycoprotein profiling in serum and plasma was also developed. Glycoprotein microarrays of enriched and separated N-linked glycoproteins from serum and plasma from normal controls and patients with pancreatic cancer and colorectal cancer were generated. The specific sugar moieties on glycans were assessed using biotinylated lectins coupled with Alexa-flor conjugated streptavidin. In both cancers sialylation and fucosylation changes were dominant. Principal component analysis and hierarchical clustering analysis showed that this strategy successfully classified serum/plasma groups based on overall glycan expression profiles. The utility of protein microarrays for identifying potential markers of pancreatic cancer was also explored. Proteins from MIAPACA, a pancreatic cancer cell line, were fractionated in 2 dimensions and arrayed on nitrocellulose slides. The slides were hybridized with multiple serum samples from normal controls and patients diagnosed with pancreatic cancer in order to find specific cancer proteins that elicited an antigen-antibody response to the serum samples. Wilcoxon rank sum tests followed by the |
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Bruise Relief Ultra, Super Hydrating serum $14.99 Ultra, Super Hydrating serum |
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Circulating Nucleic Acids in Plasma or Serum $53.95 Used – Free DNA present in both healthy and diseased human plasma has been found to express specific point mutations that may serve as diagnostic signposts–perhaps to reliable, non-invasive tests for breast and lung cancer, hematopoietic malignancies, colorectal or pancreatic carcinoma, and other tumors. In another reserch area, fetal DNA has been detected in maternal serum which presents an early-horizon alternative in utero test for gender. A parallel discovery of rearranged immunoglobulin he |
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Circulating Nucleic Acids in Plasma or Serum $35.99 Used – Free DNA present in both healthy and diseased human plasma has been found to express specific point mutations that may serve as diagnostic signposts–perhaps to reliable, non-invasive tests for breast and lung cancer, hematopoietic malignancies, colorectal or pancreatic carcinoma, and other tumors. In another reserch area, fetal DNA has been detected in maternal serum which presents an early-horizon alternative in utero test for gender. A parallel discovery of rearranged immunoglobulin he |
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Circulating Nucleic Acids in Plasma or Serum $111.5 New – Free DNA present in both healthy and diseased human plasma has been found to express specific point mutations that may serve as diagnostic signposts–perhaps to reliable, non-invasive tests for breast and lung cancer, hematopoietic malignancies, colorectal or pancreatic carcinoma, and other tumors. In another reserch area, fetal DNA has been detected in maternal serum which presents an early-horizon alternative in utero test for gender. A parallel discovery of rearranged immunoglobulin hea |
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Colorescience – The Pink Kit $60 Colorescience PRO is dedicated to the awareness, education and research for breast cancer. A portion of the proceeds from this kit will be donated to breast cancer research. We appreciate your support in the purchase of this kit and encourage you to help local groups across the country. Free of talc, mineral oil, harsh preservatives, drying alcohols, emulsifiers, dyes, perfumes and other ingredients found in traditional lines, Colorescience PRO gives you beautiful results without disrupting the skin. Colorescience products fuse all of the beauty and fun of makeup with the benefits and efficacy of skincare. Colorescience fashion forward colores give you immediate beauty benefits while premium ingredients work synergistically to create the best skin solution. With Colorescience PRO, looking good is now good for your skin! Colorescience The Pink Kit includes: Colorescience Crystalescience Lip Serum Wand (0.13 oz.) Colorescience Genie Colore Think Pink (2 g) Colorescience Genie Colore In My Pink Cadillac (2 g) Colorescience Achromatherapy Gem Spritzers Incredible Romantic (4 oz.) |
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Dietary lutein modulates expression of prostate cancer biomarker genes in human prostate cancer cell line. $49.99 Prostate cancer is the second leading cause of death from malignancies in men and is the most commonly diagnosed cancer in the United States. Epidemiological studies have shown the inverse relationship between consumption of various carotenoids and the risk of prostate cancer. Lutein is a fat-soluble, oxycarotenoid present in human serum and is also present in the liver, colon, lung and prostate tissues. Lutein is not synthesized by the human body and is primarily consumed from dark-green leafy vegetables such as kale and spinach, as well as from egg yolks, avocado, corn and fruits like orange and kiwi. Lutein has gained popularity through its role in preventing age-related macular degeneration (AMD). Anti-inflammatory activity of lutein has also been the focus of a number of in vitro and in vivo studies. Recently much attention has focused on the role of lutein against various cancers including prostate cancer, however no mechanism of action was determined.;Our objective is to determine whether lutein modulates prostate cancer biomarker genes in hormone refractory prostate cancer (PC-3) cell lines using Oligo GEArrayRTM DNA Microarray, which contains 263 genes involved in the progression and diagnosis of prostate cancer. PC-3 cells were treated with 10 muM non-toxic concentrations of lutein as determined by MTT cell viability assay. Isolated RNA was reverse-transcribed to cDNA, transcribed to cRNA and hybridized with microarrays. Microarray results demonstrated the down-regulation of epidermal growth factor receptor (EGFR), insulin-like growth factor 1 receptor (IGF1R), breast cancer gene 1 (BRCA1), cyclin dependant kinase 5 (CDK5), kallikrein 14 (KLK14) and prostate cancer antigen 3 (PCA3). Microarray results also showed the up-regulation of ras association domain family member 1 (RASSF1) and glutathione S-transferase pi 1 (GSTP1). Modulated genes were validated by Real-Time PCR and demonstrated down-regulation of IGF1R, EGFR, BRCA1, CDK5, KLK14 and PCA3 by 83%, |
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Dietary lutein modulates expression of prostate cancer biomarker genes in human prostate cancer cell line. $49.99 Prostate cancer is the second leading cause of death from malignancies in men and is the most commonly diagnosed cancer in the United States. Epidemiological studies have shown the inverse relationship between consumption of various carotenoids and the risk of prostate cancer. Lutein is a fat-soluble, oxycarotenoid present in human serum and is also present in the liver, colon, lung and prostate tissues. Lutein is not synthesized by the human body and is primarily consumed from dark-green leafy vegetables such as kale and spinach, as well as from egg yolks, avocado, corn and fruits like orange and kiwi. Lutein has gained popularity through its role in preventing age-related macular degeneration (AMD). Anti-inflammatory activity of lutein has also been the focus of a number of in vitro and in vivo studies. Recently much attention has focused on the role of lutein against various cancers including prostate cancer, however no mechanism of action was determined.;Our objective is to determine whether lutein modulates prostate cancer biomarker genes in hormone refractory prostate cancer (PC-3) cell lines using Oligo GEArrayRTM DNA Microarray, which contains 263 genes involved in the progression and diagnosis of prostate cancer. PC-3 cells were treated with 10 muM non-toxic concentrations of lutein as determined by MTT cell viability assay. Isolated RNA was reverse-transcribed to cDNA, transcribed to cRNA and hybridized with microarrays. Microarray results demonstrated the down-regulation of epidermal growth factor receptor (EGFR), insulin-like growth factor 1 receptor (IGF1R), breast cancer gene 1 (BRCA1), cyclin dependant kinase 5 (CDK5), kallikrein 14 (KLK14) and prostate cancer antigen 3 (PCA3). Microarray results also showed the up-regulation of ras association domain family member 1 (RASSF1) and glutathione S-transferase pi 1 (GSTP1). Modulated genes were validated by Real-Time PCR and demonstrated down-regulation of IGF1R, EGFR, BRCA1, CDK5, KLK14 and PCA3 by 83%, |
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Establishment Of A Diagnostic Test For The Detection Of Tumor Markers $66.99 Colorectal and breast cancer are the most common cancer types worldwide and they continue to be a serious public health problem. Early detection and diagnosis are of great importance in cancer management. At present, diagnostic blood tests are based on detection of tumor-associated markers such as CEA, PSA, AFP, and others. The lack of sensitivity and specificity of these markers prevents their general use in cancer screening of an average risk population. Therefore, new cancer biomarkers or better screening methods are necessary to improve the diagnostics of the disease. This work was directed to establishment of a diagnostic, ELISA-based test to identify and validate new serum markers, such as ecPKA and NNMT, potential candidates for detection of early human breast and colorectal neoplasm. This specific auto-antibody ELISA is thought to identify the cancer antigens by detecting the presence of auto-antibodies against the tumor proteins in human serum. In conclusion it has been showed that anti-ecPKA auto-antibody ELISA is functional and easy to perform and it could have a promising role in early diagnostic/prognostic of other cancer types. |
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Estradiol effectively inhibits the growth of tamoxifen-resistant T47D:A18/PKCalpha breast cancer. $49.99 Protein kinase C alpha (PKCalpha) overexpression in a hormone dependent breast cancer cell line T47D:A18 results in autonomous growth and tamoxifen (TAM) resistance both in vitro and in vivo. By examining PKCalpha expression in biopsies from thirty patients, we found that PKCalpha overexpression is relevant in TAM-resistant breast cancer in the clinic, indicating PKCalpha may be a potential marker for TAM-resistant breast cancer. Most notably, 17beta estradiol (E2) inhibits T47D:A18/PKCalpha cell growth in vivo but not on plastic. We observed that growth in Matrigel, a reconstituted basement membrane, was sufficient for E2 to exhibit the inhibitory effect, therefore the extracellular matrix might be required for the E2-inhibitory action. Then we applied Matrigel 3-dimensional cell culture to study the mechanisms of the E2-inhibitory effect. Knock-down of Fas in T47D:A18/PKCalpha cells reduced the E2-inhibitory effect on the colony formation in Matrigel, indicating Fas/FasL apoptotic pathway contributes in the E2-inhibited cell growth. Furthermore, we applied fulvestrant, a pure antiestrogen that induces estrogen receptor (ER) degradation, in the tumor growth studies and found that fulvestrant can abolish the inhibitory effect of E2 on T47D/PKCalpha tumor growth and E2-induced Fas/FasL upregulation in vivo. This result suggests that the ER is likely to participate in the mechanism of E2 inhibitory effect. To determine whether the membrane associated ER is involved in E2-inhibited T47D:A18/PKCalpha cell growth, we treated the cells grown in Matrigel with the cell membrane impermeable bovine serum albumin conjugated E2 (E2-BSA) and found that both E2 and E2-BSA conjugate have a similar inhibitory effect on T47D:A18/PKCalpha cell growth in Matrigel. These results indicate that the membrane associated ER may mediate the observed E2-inhibitory effects. Taken together, our findings suggest that Fas/FasL pathway contributes to E2-induced apoptosis in T47D:A18/PKCalpha |
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Estradiol effectively inhibits the growth of tamoxifen-resistant T47D:A18/PKCalpha breast cancer. $49.99 Protein kinase C alpha (PKCalpha) overexpression in a hormone dependent breast cancer cell line T47D:A18 results in autonomous growth and tamoxifen (TAM) resistance both in vitro and in vivo. By examining PKCalpha expression in biopsies from thirty patients, we found that PKCalpha overexpression is relevant in TAM-resistant breast cancer in the clinic, indicating PKCalpha may be a potential marker for TAM-resistant breast cancer. Most notably, 17beta estradiol (E2) inhibits T47D:A18/PKCalpha cell growth in vivo but not on plastic. We observed that growth in Matrigel, a reconstituted basement membrane, was sufficient for E2 to exhibit the inhibitory effect, therefore the extracellular matrix might be required for the E2-inhibitory action. Then we applied Matrigel 3-dimensional cell culture to study the mechanisms of the E2-inhibitory effect. Knock-down of Fas in T47D:A18/PKCalpha cells reduced the E2-inhibitory effect on the colony formation in Matrigel, indicating Fas/FasL apoptotic pathway contributes in the E2-inhibited cell growth. Furthermore, we applied fulvestrant, a pure antiestrogen that induces estrogen receptor (ER) degradation, in the tumor growth studies and found that fulvestrant can abolish the inhibitory effect of E2 on T47D/PKCalpha tumor growth and E2-induced Fas/FasL upregulation in vivo. This result suggests that the ER is likely to participate in the mechanism of E2 inhibitory effect. To determine whether the membrane associated ER is involved in E2-inhibited T47D:A18/PKCalpha cell growth, we treated the cells grown in Matrigel with the cell membrane impermeable bovine serum albumin conjugated E2 (E2-BSA) and found that both E2 and E2-BSA conjugate have a similar inhibitory effect on T47D:A18/PKCalpha cell growth in Matrigel. These results indicate that the membrane associated ER may mediate the observed E2-inhibitory effects. Taken together, our findings suggest that Fas/FasL pathway contributes to E2-induced apoptosis in T47D:A18/PKCalpha |
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Flaxseed Lignans: Properties and Health Benefits $59.99 The flaxseed (Linum usitatissimum L.) lignans secoisolariciresinol (SECO) and its diglucoside secoisolariciresinol diglucoside (SDG) are reported to have a number of health benefits including reduction of serum cholesterol levels, delay in the onset of type II diabetes and decreased formation of breast, prostate and colon cancers. The health benefits of SECO and SDG may be partially attributed to their antioxidant properties. To better understand their antioxidant properties, SECO and SDG are oxidized and the major lignan radical- scavenging oxidation products and their formation over time can be determined. Flaxseed lignans act as chain breaking antioxidants in food and biological systems. This indicates that flaxseed lignans may be useful as alternative natural antioxidant preservatives and may be applicable in this role in vegetable oils and in other oil-based foods to provide additional health benefits as antioxidant or antiestrogenic compounds. |
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Flaxseed Lignans: Properties and Health Benefits $62 New – The flaxseed (Linum usitatissimum L.) lignans secoisolariciresinol (SECO) and its diglucoside secoisolariciresinol diglucoside (SDG) are reported to have a number of health benefits including reduction of serum cholesterol levels, delay in the onset of type II diabetes and decreased formation of breast, prostate and colon cancers. The health benefits of SECO and SDG may be partially attributed to their antioxidant properties. To better understand their antioxidant properties, SECO and SDG |
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Flaxseed Lignans: Properties and Health Benefits $62 Used – The flaxseed (Linum usitatissimum L.) lignans secoisolariciresinol (SECO) and its diglucoside secoisolariciresinol diglucoside (SDG) are reported to have a number of health benefits including reduction of serum cholesterol levels, delay in the onset of type II diabetes and decreased formation of breast, prostate and colon cancers. The health benefits of SECO and SDG may be partially attributed to their antioxidant properties. To better understand their antioxidant properties, SECO and SDG |
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Jarrow Formulas Lactoferrin 250mg 60 capsules $14.68 Authorized Vendor for Lactoferrin. Jarrow FORMULAS Lactoferrin is an important immune supporting glycoprotein that is found in breast milk, tears, and other body fluids. One of the biological activities of lactoferrin comes from its powerful ability to bind iron (300 times that of serum transferrin). Moreover, digestion of lactoferrin by gastric pepsin liberates the immune supporting peptide lactoferricin B. Lactoferrin also benefits intestinal health by promoting the growth of beneficial bacteria.. |
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Lutein 20 mg 60 Softgels by Nutricology/ Allergy Research Group $15.67 Authorized Vendor for Lutein. Lutein belongs to the carotenoid family of antioxidants. In the body lutein has been found in the eye, brain, breast and cervix. Research has shown lutein to be supportive for vision health. In the eye, it is found mainly in the macular region, the entire retina, ciliary iris bodies and lens. As an antioxidant, lutein supports the body in protecting macular tissue from photo-oxidation by filtering blue light and relieving oxidative damage by free radical quenching. Adequate levels of lutein in the eye may potentially be supportive in the absorption and dissipation of damaging UV radiation. Research involving lutein supplementation has shown a 130% increase in serum levels of lutein. Furthermore, most subjects had an increase in their macular pigment density as a result of the supplementation.. |
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Mama Mio – ZAP Emergency Repair Kit $130 The time has come to get your body back – this is the total skincare solution to help regain smooth toned skin. Alas, cellulite, excess curve and sagging skin tend to be the less adorable side effects of motherhood and aging. This New Mama Mio Emergency Repair Kit contains Mama Mio Tummy Toner (100ml/3.4 oz.) – Everyone needs a little boost for bikini confidence, whether it’s pregnancy, weight loss or aging we all yearn for tight toned skin of yesteryear. Mama Mio Shrink To Fit Cream (100 ml/3.4 oz.) – A sink-in-quick serum cream, packed with radically effective ingredients to help reduce the appearance of cellulite, restore elasticity, reduce water retention and sponginess, and increase firmness. ‘Honey, I shrank my hips!’ Tummy Toner works in three simple stages: 1. Exfoliate – removing dead and damaged skin cells on the surface, enhancing skin smoothness and encouraging the development of newer cells. 2. Intensely Moisturise – plumping up the skin surface smoothing out the crepeyness from beneath. 3. Tighten and tone – lifts and tightens, giving your skin a more toned, youthful and fresh appearance. Shrink To Fit Cream has six key ingredients that collectively zap cellulite by breaking down fat stored in fat cells and preventing new fat cells from forming. Shrink To Fit Cream boosts circulation, reduces water retention, and firms skin all whilst fighting free radicals. What a superhero! Directions: If you want to make a difference you have to commit. This is not a one night stand. Use Mama Mio Shrink To Fit Cream on all trouble spots – tummy, upper arms, thighs and bottom – massaging for 20 seconds twice a day for 30 days. Gently massage Mama Mio Tummy Toner from below the breast to across the entire abdomen, use it twice daily and use 6-8 weeks for maximum results. Net Weight: Please see individual items. |
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Mechanisms of estrogen carcinogenesis in human breast epithelial cells. $49.99 Breast cancer remains the primary cause of cancer-related death in women. In an effort to prevent breast cancer, elucidation of the mechanism of estrogen carcinogenesis is of immense importance. Cellular transformation (using MCF-10A cells as model system), caused by estrogen oxidative metabolites reacting with DNA, showed an increased carcinogenic potential for the endogenous estrogens compared to the exogenous HRT estrogens.;Improved solid-phase extraction and MS methods were used to isolate the depurinating DNA adducts generated from catechol estrogen quinones reacting with the purine bases of DNA. The correlation established between detected depurinating adducts and cellular transformation ability of estrogens suggests that DNA damage from depurination can serve as a biomarker in breast cancer. SERMs efficiently prevented cellular transformation caused by estrogen. For the first time we are reporting the ability of a SERM (DMA) to modulate estrogen metabolism towards favoring formation of a lesser genotoxic C2-catechol metabolite in MCF-10A cells.;Finally, we reported and characterized a novel signaling in human breast epithelial cells (MCF-10A) involving estrogen and nitric oxide. This is the first report of the interdependence between estrogen and NO signaling in maintaining cell viability. Either estrogen or NOS inhibitors alone have no significant effect, while the combination of estrogen and impaired NO signaling can amplify apoptosis induced by serum deprivation and growth factor withdrawal. The regulatory effects of estrogen reported here could represent a general mechanism by which normal cell physiology is fine tuned by NO signaling under stressed conditions. |
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Mechanisms of estrogen carcinogenesis in human breast epithelial cells. $49.99 Breast cancer remains the primary cause of cancer-related death in women. In an effort to prevent breast cancer, elucidation of the mechanism of estrogen carcinogenesis is of immense importance. Cellular transformation (using MCF-10A cells as model system), caused by estrogen oxidative metabolites reacting with DNA, showed an increased carcinogenic potential for the endogenous estrogens compared to the exogenous HRT estrogens.;Improved solid-phase extraction and MS methods were used to isolate the depurinating DNA adducts generated from catechol estrogen quinones reacting with the purine bases of DNA. The correlation established between detected depurinating adducts and cellular transformation ability of estrogens suggests that DNA damage from depurination can serve as a biomarker in breast cancer. SERMs efficiently prevented cellular transformation caused by estrogen. For the first time we are reporting the ability of a SERM (DMA) to modulate estrogen metabolism towards favoring formation of a lesser genotoxic C2-catechol metabolite in MCF-10A cells.;Finally, we reported and characterized a novel signaling in human breast epithelial cells (MCF-10A) involving estrogen and nitric oxide. This is the first report of the interdependence between estrogen and NO signaling in maintaining cell viability. Either estrogen or NOS inhibitors alone have no significant effect, while the combination of estrogen and impaired NO signaling can amplify apoptosis induced by serum deprivation and growth factor withdrawal. The regulatory effects of estrogen reported here could represent a general mechanism by which normal cell physiology is fine tuned by NO signaling under stressed conditions. |
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Membrane progestin receptor expression, signaling and function in reproductive somatic cells of female vertebrates. $49.99 The goal of the current research was to examine the expression, signaling and function of the membrane progestin receptors (mPRs) in the ovarian follicular cells of the Atlantic croaker (Micropogonias undulatus) and in human breast cancer cells. Multiple studies have examined the role of mPRs in the germ cells of several vertebrate classes, yet few studies have examined the role of the mPRs in the somatic cells of reproductive tissues. Therefore this research examines the mechanism of mPR action and its function in somatic cells of female reproductive tissues.;Results from studies on the expression, localization and signaling of the mPRalpha in co-cultures of granulosa and theca cells from the croaker suggest that the mPRalpha is localized to the plasma membrane of both cell types and that the mPRalpha is associated with and signals via pertussis toxin-sensitive inhibitory G proteins to decrease intracellular cAMP and activate ERK. In addition, exposure of follicular co-cultures to progestins that activate the mPRalpha results in a decrease in serum starvation-induced cell death which is not replicated by progestins which activate the nuclear progestin receptor (nPR), indicating mPR mediation.;Similar studies in two immortalized human breast cancer cell lines, MDA-MB-468 and SKBR3, suggest that the mPRalpha is also present in the membranes of these cells and signals in human breast cancer cell lines via activation of a pertussis toxin-sensitive G protein to significantly decrease in intracellular cAMP and activate ERK. Progesterone exposure also decreased serum starvation-induced cell death in SKBR3 cells which are nPR positive and in MDA-MB-468 cells which are nPR negative. Synthetic progestins which activate the nPR but not the mPR were ineffective in inhibiting death in either cell type suggesting that the mPR is the mediator of this progestin action.;mPRalpha, mPRbeta and mPRgamma expression analysis of paired normal and malignant breast tissue biopsies from |
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Membrane progestin receptor expression, signaling and function in reproductive somatic cells of female vertebrates. $49.99 The goal of the current research was to examine the expression, signaling and function of the membrane progestin receptors (mPRs) in the ovarian follicular cells of the Atlantic croaker (Micropogonias undulatus) and in human breast cancer cells. Multiple studies have examined the role of mPRs in the germ cells of several vertebrate classes, yet few studies have examined the role of the mPRs in the somatic cells of reproductive tissues. Therefore this research examines the mechanism of mPR action and its function in somatic cells of female reproductive tissues.;Results from studies on the expression, localization and signaling of the mPRalpha in co-cultures of granulosa and theca cells from the croaker suggest that the mPRalpha is localized to the plasma membrane of both cell types and that the mPRalpha is associated with and signals via pertussis toxin-sensitive inhibitory G proteins to decrease intracellular cAMP and activate ERK. In addition, exposure of follicular co-cultures to progestins that activate the mPRalpha results in a decrease in serum starvation-induced cell death which is not replicated by progestins which activate the nuclear progestin receptor (nPR), indicating mPR mediation.;Similar studies in two immortalized human breast cancer cell lines, MDA-MB-468 and SKBR3, suggest that the mPRalpha is also present in the membranes of these cells and signals in human breast cancer cell lines via activation of a pertussis toxin-sensitive G protein to significantly decrease in intracellular cAMP and activate ERK. Progesterone exposure also decreased serum starvation-induced cell death in SKBR3 cells which are nPR positive and in MDA-MB-468 cells which are nPR negative. Synthetic progestins which activate the nPR but not the mPR were ineffective in inhibiting death in either cell type suggesting that the mPR is the mediator of this progestin action.;mPRalpha, mPRbeta and mPRgamma expression analysis of paired normal and malignant breast tissue biopsies from |
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Rexinoids And Celecoxib In Breast Cancer Chemoprevention And Serum Biomarker Identification. $69 Stephan Woditschka,Paperback, English-language edition,Pub by ProQuest, UMI Dissertation Publishing |
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Rexinoids and celecoxib in breast cancer chemoprevention and serum biomarker identification. $49.99 The field of chemoprevention represents a promising aspect in the battle against breast cancer. All animal experiments were conducted using neu-induced retroviral rat models of mammary carcinogenesis. In intact rats of this model, approximately 50% of mammary carcinomas are hormonally responsive and can be prevented by anti-estrogenic tamoxifen-treatment. The carcinomas of ovariectomized rats are hormonally non-responsive and cannot be prevented by tamoxifen. We evaluated the cyclooxygenase-2 inhibitor celecoxib and the retinoic X receptor-selective retinoids (rexinoids) LG100268 and targretin (LGD1069, bexarotene) for their efficacyto prevent mammary cancer in our neu -induced rat models. Targretin-treatment resulted in similar reductions in tumor multiplicity (84% and 86%) in intact and ovariectomized rat models, respectively, suggesting that the chemoprevention properties of bexarotene are independent of ovarian hormone signaling. The chemopreventive effects of celecoxib are limited to hormonally responsive tumors and parallel those of tamoxifen in both hormonal models. No synergistic or additive effects were observed in celecoxib/tamoxifen combination diet-treated rats. We developed a short-term prevention model, which represents a cost-effective methodology to assess a compound’s efficacy to prevent both hormonally responsive and non-responsive in situ carcinomas. The preventive effects of tamoxifen, celecoxib and targretin on in situ carcinomas recapitulate those observed in mammary carcinomas in our long-term model. We aimed to identify secreted biomarkers that can be used as surrogate, intermediate endpoints for evaluating the efficacy of chemopreventive agents. Using Affymetrix microarray technology, a set of 1163 genes was identified to be differentially expressed in response to rexinoid treatment. Within this set, secreted proteins were identified by informatic screens. The expression of selected candidates was assessed under different estrogen signaling |
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Rexinoids and celecoxib in breast cancer chemoprevention and serum biomarker identification. $49.99 The field of chemoprevention represents a promising aspect in the battle against breast cancer. All animal experiments were conducted using neu-induced retroviral rat models of mammary carcinogenesis. In intact rats of this model, approximately 50% of mammary carcinomas are hormonally responsive and can be prevented by anti-estrogenic tamoxifen-treatment. The carcinomas of ovariectomized rats are hormonally non-responsive and cannot be prevented by tamoxifen. We evaluated the cyclooxygenase-2 inhibitor celecoxib and the retinoic X receptor-selective retinoids (rexinoids) LG100268 and targretin (LGD1069, bexarotene) for their efficacyto prevent mammary cancer in our neu -induced rat models. Targretin-treatment resulted in similar reductions in tumor multiplicity (84% and 86%) in intact and ovariectomized rat models, respectively, suggesting that the chemoprevention properties of bexarotene are independent of ovarian hormone signaling. The chemopreventive effects of celecoxib are limited to hormonally responsive tumors and parallel those of tamoxifen in both hormonal models. No synergistic or additive effects were observed in celecoxib/tamoxifen combination diet-treated rats. We developed a short-term prevention model, which represents a cost-effective methodology to assess a compound’s efficacy to prevent both hormonally responsive and non-responsive in situ carcinomas. The preventive effects of tamoxifen, celecoxib and targretin on in situ carcinomas recapitulate those observed in mammary carcinomas in our long-term model. We aimed to identify secreted biomarkers that can be used as surrogate, intermediate endpoints for evaluating the efficacy of chemopreventive agents. Using Affymetrix microarray technology, a set of 1163 genes was identified to be differentially expressed in response to rexinoid treatment. Within this set, secreted proteins were identified by informatic screens. The expression of selected candidates was assessed under different estrogen signaling |
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StriVectin Hydro-Thermal Bust Beautification Serum $165 Buy Klein Becker Bust Treatments – StriVectin Hydro-Thermal Bust Beautification Serum 100ml/3.4oz. How-to-Use: Step 1: Shake well before using.Step 2: Begin with clean, dry skin.Step 3: Apply a small amount of StriVectin Bust Beautification Serum into the palm of your hand (a pea-sized amount, or as needed).nbsp; Use sparingly.nbsp; The serum is extremely concentrated.Step 4: Massage the serum into each breast, beginning at the top |
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Talika – Bust Serum 2.0 $49 Talika laboratories, experts in specific care, have created Bust Serum, a comprehensive beauty package giving volume, lift and firmness to the breast. Volume: gain one cup size in 6 weeks The breasts are composed of varying amounts of fatty tissue which gives them shape and volume. Thanks to the virtues of mukul bark extract that has been used for centuries in Indian Ayurvedic medicine, Bust Serum fosters a targeted storage of triglycerides, thereby increasing breast volume. Tests have proved that 80% of women saw an increase of 2 to 4 cm (1 to 1 3/4 in) in 6 weeks. Breast lift: +18% The breasts are attached to the thorax by ligaments (Cooper’s ligaments). With absolutely no muscle, their only support is the skin. Volume and weight variations erode skin elasticity, triggering a loss in curve and sagging.Thanks to the extract of kigelia africana , Bust Serum prevents the tissue from sagging and improves bust firmness and appearance. Clinical trials have shown +18% in breast lift. Firmness The combination of kigelia africana, mukul bark extract, oat extract, peptides, raspberry seed oil from Chile and hyaluronic acid strengthens the skin’s binding and hence tonicity, thereby tangibly improving its elasticity by 70%. Your breasts will be better maintained and developed as result. Directions: Apply Bust Serum daily, morning or evening, to the base of the breasts and then massage in wide figure 8 movements from below the breast upto the neck line. Net Weight: 50 ml/1.7 oz. |
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The Effect of Phospholipase D on Tgf-Beta Signaling in Cancer Survival. $79.63 Used – MDA-MB-231 human breast cancer cells have a survival signal generated by phospholipase D (PLD) that involves the activation of the mammalian target of rapamycin (mTOR) and mitogenic activated protein kinase (MAPK). In the absence of serum, rapamycin induces apoptosis in MDA-MB-231 human breast cancer cells. However, in the presence of serum, rapamycin induces G1 cell cycle arrest — indicating that a factor(s) in serum suppresses rapamycin-induced apoptosis. We find that transforming grow |
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The Needs and Development of Physical Standards for Medical Diagnostics and Research: Book edition of Cancer Biomarkers $80 For clinical chemistry and biomedical applications, reference materials (RMs) or certified reference materials (CRMs) may take the form of neat materials of assessed purity, or solutions of analytes. A Standard Reference Material® (SRM) is a CRM issued by the United States National Institute of Standards and Technology (NIST). As SRMs are precious commodities, they typically are not intended for routine clinical or experimental applications as controls. Intended use descriptions often accompany supporting documentation of such standards. As part of continued NIST commitment to healthcare, recent NIST workshops have addressed standards and technology in areas such as nanotechnology and early cancer detection, HER2 testing of breast cancer, gene expression and serum proteomics for early cancer detection. Standards arise in response to clinical needs. Working in partnership with the standards user communities, NIST serves the national measurements community and has the specific federally mandated responsibility to meet high-priority reference material needs. |
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The effect of phospholipase D on TGF-beta signaling in cancer survival. $49.99 MDA-MB-231 human breast cancer cells have a survival signal generated by phospholipase D (PLD) that involves the activation of the mammalian target of rapamycin (mTOR) and mitogenic activated protein kinase (MAPK). In the absence of serum, rapamycin induces apoptosis in MDA-MB-231 human breast cancer cells. However, in the presence of serum, rapamycin induces G1 cell cycle arrest — indicating that a factor(s) in serum suppresses rapamycin-induced apoptosis. We find that transforming growth factor-beta (TGF-beta) suppresses rapamycin-induced apoptosis in serum-deprived MDA-MB-231 cells in a protein kinase Cdelta (PKCdelta)-dependent manner. Importantly, if TGF-beta signaling or PKCdelta was suppressed, rapamycin induced apoptosis rather than G1 arrest in the presence of serum. If cells were allowed to progress into S-phase, rapamycin induced apoptosis in the presence of serum. We also examined the effect of rapamycin on cancer cell lines harboring genetic defects in TGF-beta signaling, and as expected, rapamycin induced apoptosis in these cells in the presence of either serum or TGF-beta. Thus, in the absence of TGF-beta signaling, rapamycin becomes cytotoxic rather than cytostatic.;MDA-MB-231 breast cancer cells are resistant to the growth arresting effects of TGF-beta. Since mTOR is a target of PLD signals and mTOR suppresses TGF-beta signaling, we investigated whether the elevated PLD activity in MDA-MB-231 cells is critical for the reported suppression of TGF-beta signaling in these cells. Suppression of PLD activity and/or expression resulted in increased activation of Smads and in addition suppressed phosphorylation of Smad2 on sites that are phosphorylated by MAP kinase and negatively regulate TGF-beta signaling. Suppression of PLD also led to a predictable response of known TGF-beta downstream targets like p21Cip1, p27 Kip1and pRb.;The data presented in this work indicate that the suppressed TGF-beta signaling in MDA-MB-231 cells is due to elevated PLD |
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The effect of phospholipase D on TGF-beta signaling in cancer survival. $108 MDA-MB-231 human breast cancer cells have a survival signal generated by phospholipase D (PLD) that involves the activation of the mammalian target of rapamycin (mTOR) and mitogenic activated protein kinase (MAPK). In the absence of serum, rapamycin induces apoptosis in MDA-MB-231 human breast cancer cells. However, in the presence of serum, rapamycin induces G1 cell cycle arrest — indicating that a factor(s) in serum suppresses rapamycin-induced apoptosis. We find that transforming growth factor-beta (TGF-beta) suppresses rapamycin-induced apoptosis in serum-deprived MDA-MB-231 cells in a protein kinase Cdelta (PKCdelta)-dependent manner. Importantly, if TGF-beta signaling or PKCdelta was suppressed, rapamycin induced apoptosis rather than G1 arrest in the presence of serum. If cells were allowed to progress into S-phase, rapamycin induced apoptosis in the presence of serum. We also examined the effect of rapamycin on cancer cell lines harboring genetic defects in TGF-beta signaling, and as expected, rapamycin induced apoptosis in these cells in the presence of either serum or TGF-beta. Thus, in the absence of TGF-beta signaling, rapamycin becomes cytotoxic rather than cytostatic.;MDA-MB-231 breast cancer cells are resistant to the growth arresting effects of TGF-beta. Since mTOR is a target of PLD signals and mTOR suppresses TGF-beta signaling, we investigated whether the elevated PLD activity in MDA-MB-231 cells is critical for the reported suppression of TGF-beta signaling in these cells. Suppression of PLD activity and/or expression resulted in increased activation of Smads and in addition suppressed phosphorylation of Smad2 on sites that are phosphorylated by MAP kinase and negatively regulate TGF-beta signaling. Suppression of PLD also led to a predictable response of known TGF-beta downstream targets like p21Cip1, p27 Kip1and pRb.;The data presented in this work indicate that the suppressed TGF-beta signaling in MDA-MB-231 cells is due to elevated PLD |
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The effect of phospholipase D on TGF-beta signaling in cancer survival. $49.99 MDA-MB-231 human breast cancer cells have a survival signal generated by phospholipase D (PLD) that involves the activation of the mammalian target of rapamycin (mTOR) and mitogenic activated protein kinase (MAPK). In the absence of serum, rapamycin induces apoptosis in MDA-MB-231 human breast cancer cells. However, in the presence of serum, rapamycin induces G1 cell cycle arrest — indicating that a factor(s) in serum suppresses rapamycin-induced apoptosis. We find that transforming growth factor-beta (TGF-beta) suppresses rapamycin-induced apoptosis in serum-deprived MDA-MB-231 cells in a protein kinase Cdelta (PKCdelta)-dependent manner. Importantly, if TGF-beta signaling or PKCdelta was suppressed, rapamycin induced apoptosis rather than G1 arrest in the presence of serum. If cells were allowed to progress into S-phase, rapamycin induced apoptosis in the presence of serum. We also examined the effect of rapamycin on cancer cell lines harboring genetic defects in TGF-beta signaling, and as expected, rapamycin induced apoptosis in these cells in the presence of either serum or TGF-beta. Thus, in the absence of TGF-beta signaling, rapamycin becomes cytotoxic rather than cytostatic.;MDA-MB-231 breast cancer cells are resistant to the growth arresting effects of TGF-beta. Since mTOR is a target of PLD signals and mTOR suppresses TGF-beta signaling, we investigated whether the elevated PLD activity in MDA-MB-231 cells is critical for the reported suppression of TGF-beta signaling in these cells. Suppression of PLD activity and/or expression resulted in increased activation of Smads and in addition suppressed phosphorylation of Smad2 on sites that are phosphorylated by MAP kinase and negatively regulate TGF-beta signaling. Suppression of PLD also led to a predictable response of known TGF-beta downstream targets like p21Cip1, p27 Kip1and pRb.;The data presented in this work indicate that the suppressed TGF-beta signaling in MDA-MB-231 cells is due to elevated PLD |
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The effects of anthropometry and angiogenesis on breast cancer etiology. $49.99 Factors such as mammographic breast density and angiogenesis may be related to breast cancer development, though numerous questions about the etiologic mechanisms remain. Percent density is positively associated with breast cancer risk, yet is negatively associated with another breast cancer risk factor, body mass index (BMI). Vascular endothelial growth factor (VEGF) is a primary regulator of angiogenesis, yet its relationship to breast cancer risk is unclear. We evaluated the longitudinal association between BMI and breast density in the Study of Women’s Health Across the Nation (SWAN) Mammographic Density Substudy (N=834). Using adjusted random intercept models, changes in BMI were not associated with changes in dense breast area (beta=-0.0105, p=0.34), but were strongly negatively associated with changes in percent density (beta=-1.18, p<0.001). Thus, effects of changes in anthropometry on percent breast density may reflect effects on non-dense tissue, rather than on the dense tissue where cancers arise. Breast density was measured from routine screening mammograms which were not timed with SWAN visits. We developed a method to align the off-schedule mammogram data to the study visit times using linear interpolation with multiple imputation. Our method was shown to be valid, with an average bias for dense breast area of 0.11 cm 2. In the random intercept models, use of a simple matching algorithm to estimate breast density produced different (beta=-0.0155, p=0.04), and likely incorrect, results. Our linear interpolation with multiple imputations method may be applicable to other longitudinal datasets with important data collected off-schedule. In a separate case-control study, the Mammograms and Masses Study (MAMS), we evaluated the association between serum VEGF levels and breast cancer (N=407). Geometric mean VEGF levels were higher among cases (331.4 pg/mL) than controls (291.4 pg/mL; p=0.21). In a multivariable logistic regression model, VEGF ≥314.2 |
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The effects of anthropometry and angiogenesis on breast cancer etiology. $49.99 Factors such as mammographic breast density and angiogenesis may be related to breast cancer development, though numerous questions about the etiologic mechanisms remain. Percent density is positively associated with breast cancer risk, yet is negatively associated with another breast cancer risk factor, body mass index (BMI). Vascular endothelial growth factor (VEGF) is a primary regulator of angiogenesis, yet its relationship to breast cancer risk is unclear. We evaluated the longitudinal association between BMI and breast density in the Study of Women’s Health Across the Nation (SWAN) Mammographic Density Substudy (N=834). Using adjusted random intercept models, changes in BMI were not associated with changes in dense breast area (beta=-0.0105, p=0.34), but were strongly negatively associated with changes in percent density (beta=-1.18, p<0.001). Thus, effects of changes in anthropometry on percent breast density may reflect effects on non-dense tissue, rather than on the dense tissue where cancers arise. Breast density was measured from routine screening mammograms which were not timed with SWAN visits. We developed a method to align the off-schedule mammogram data to the study visit times using linear interpolation with multiple imputation. Our method was shown to be valid, with an average bias for dense breast area of 0.11 cm 2. In the random intercept models, use of a simple matching algorithm to estimate breast density produced different (beta=-0.0155, p=0.04), and likely incorrect, results. Our linear interpolation with multiple imputations method may be applicable to other longitudinal datasets with important data collected off-schedule. In a separate case-control study, the Mammograms and Masses Study (MAMS), we evaluated the association between serum VEGF levels and breast cancer (N=407). Geometric mean VEGF levels were higher among cases (331.4 pg/mL) than controls (291.4 pg/mL; p=0.21). In a multivariable logistic regression model, VEGF ≥314.2 |
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The effects of anthropometry and angiogenesis on breast cancer etiology. $108 Factors such as mammographic breast density and angiogenesis may be related to breast cancer development, though numerous questions about the etiologic mechanisms remain. Percent density is positively associated with breast cancer risk, yet is negatively associated with another breast cancer risk factor, body mass index (BMI). Vascular endothelial growth factor (VEGF) is a primary regulator of angiogenesis, yet its relationship to breast cancer risk is unclear. We evaluated the longitudinal association between BMI and breast density in the Study of Women’s Health Across the Nation (SWAN) Mammographic Density Substudy (N=834). Using adjusted random intercept models, changes in BMI were not associated with changes in dense breast area (beta=-0.0105, p=0.34), but were strongly negatively associated with changes in percent density (beta=-1.18, p<0.001). Thus, effects of changes in anthropometry on percent breast density may reflect effects on non-dense tissue, rather than on the dense tissue where cancers arise. Breast density was measured from routine screening mammograms which were not timed with SWAN visits. We developed a method to align the off-schedule mammogram data to the study visit times using linear interpolation with multiple imputation. Our method was shown to be valid, with an average bias for dense breast area of 0.11 cm 2. In the random intercept models, use of a simple matching algorithm to estimate breast density produced different (beta=-0.0155, p=0.04), and likely incorrect, results. Our linear interpolation with multiple imputations method may be applicable to other longitudinal datasets with important data collected off-schedule. In a separate case-control study, the Mammograms and Masses Study (MAMS), we evaluated the association between serum VEGF levels and breast cancer (N=407). Geometric mean VEGF levels were higher among cases (331.4 pg/mL) than controls (291.4 pg/mL; p=0.21). In a multivariable logistic regression model, VEGF ≥314.2 |
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The inhibition of ATM and Akt by the ATM inhibitor KU-55933 induces cell cycle arrest and apoptosis in cancer cells with over-activated Akt. $49.99 ATM (ataxia-telangiectasia, mutated) is a gene mutated in the autosomal recessive disorder ataxia telangiectasia. ATM is traditionally considered to be a signal transducer in the cellular responses to DNA damage. It has recently been demonstrated that ATM responds to insulin stimulation and mediates the full activation of Akt. Akt is a key signal transducer in the PI 3-kinase signaling pathway that promotes cell proliferation and cell survival. The over-expression or over-activation of Akt occurs frequently in many types of cancer, making it a valuable target for cancer therapy. Our study shows that the specific ATM inhibitor, KU-55933, effectively blocks the phosphorylation of Akt in response to insulin and IGF-I and inhibits Akt kinase activity in MDA-MB-453 breast cancer and PC-3 prostate cancer cell lines. By inhibiting Akt, KU-55933 inhibits the proliferation of both cell lines in a dose- and time-dependent manner. We further show that the inhibition of cell proliferation by KU-55933 happens through cell cycle arrest. The expression of cyclin D1, which is downstream of Akt and controls cell cycle progression, is down-regulated by KU-55933 through the inhibition of cyclin D1 synthesis. This down-regulation of cyclin D1 is not due to an increased rate of proteasomal degradation or a decreased rate of transcription. The inhibition of ATM by KU-55933 leads to the dephosphorylation of 4E-BP1 and increased interaction between 4E-BP1 and eIF-4E. This prevents protein translation initiation, which may account for decreased cyclin D1 translation. KU-55933 treatment during serum starvation triggers apoptosis, demonstrated by elevated levels of cleaved-PARP and DNA fragmentation. Our results suggest that KU-55933 may be a novel chemotherapeutic agent targeting cancer resistant to traditional chemo- or immunotherapy due to aberrant activation of Akt. Furthermore, KU-55933 abolishes the feedback activation of Akt induced by rapamycin. The combination of rapamycin with |
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The inhibition of ATM and Akt by the ATM inhibitor KU-55933 induces cell cycle arrest and apoptosis in cancer cells with over-activated Akt. $49.99 ATM (ataxia-telangiectasia, mutated) is a gene mutated in the autosomal recessive disorder ataxia telangiectasia. ATM is traditionally considered to be a signal transducer in the cellular responses to DNA damage. It has recently been demonstrated that ATM responds to insulin stimulation and mediates the full activation of Akt. Akt is a key signal transducer in the PI 3-kinase signaling pathway that promotes cell proliferation and cell survival. The over-expression or over-activation of Akt occurs frequently in many types of cancer, making it a valuable target for cancer therapy. Our study shows that the specific ATM inhibitor, KU-55933, effectively blocks the phosphorylation of Akt in response to insulin and IGF-I and inhibits Akt kinase activity in MDA-MB-453 breast cancer and PC-3 prostate cancer cell lines. By inhibiting Akt, KU-55933 inhibits the proliferation of both cell lines in a dose- and time-dependent manner. We further show that the inhibition of cell proliferation by KU-55933 happens through cell cycle arrest. The expression of cyclin D1, which is downstream of Akt and controls cell cycle progression, is down-regulated by KU-55933 through the inhibition of cyclin D1 synthesis. This down-regulation of cyclin D1 is not due to an increased rate of proteasomal degradation or a decreased rate of transcription. The inhibition of ATM by KU-55933 leads to the dephosphorylation of 4E-BP1 and increased interaction between 4E-BP1 and eIF-4E. This prevents protein translation initiation, which may account for decreased cyclin D1 translation. KU-55933 treatment during serum starvation triggers apoptosis, demonstrated by elevated levels of cleaved-PARP and DNA fragmentation. Our results suggest that KU-55933 may be a novel chemotherapeutic agent targeting cancer resistant to traditional chemo- or immunotherapy due to aberrant activation of Akt. Furthermore, KU-55933 abolishes the feedback activation of Akt induced by rapamycin. The combination of rapamycin with |
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The omega-6 and omega-3 polyunsaturated fatty acids and modifiable breast cancer risk factors. $49.99 Experimental evidence suggests that omega-6 (n-6) fatty acids have mammary tumor promoting effects whereas omega-3 (n-3) fatty acids inhibit tumor growth. These two families of fatty acids may influence breast cancer development by impacting prostaglandin E2 (PGE2) formation and consequently estradiol synthesis. Whether this effect on estrogen production can be observed in the circulation or in breast tissue, as reflected on a mammogram, is unknown. Therefore, using fatty acids in erythrocytes as a biomarker of recent dietary intake, we sought to establish the relationship between the n-6 and n-3 fatty acids with both serum estradiol and mammographic breast density, two well-established modifiable breast cancer risk factors. We hypothesized that n-6 fatty acids are positively related and n-3 fatty acids negatively related to both risk factors. Nonsteroidal anti-inflammatory drugs (NSAIDs) also inhibit PGE2 formation, therefore we further hypothesized that estradiol levels would be lower among NSAID users. NSAID data was not available at the time of mammogram; hence the relationship between NSAID use and mammographic density could not accurately be assessed. To test our hypotheses we conducted several investigations ancillary to the Mammograms and Masses Study (MAMS), a case control study of the determinants of mammographic breast density. Participants were eligible for this compilation of studies if they were breast cancer-free, postmenopausal and not taking exogenous hormones. We observed significantly lower levels of serum estradiol among current users of NSAIDs as compared to non-users of NSAIDs. Further, as hypothesized, estradiol concentration decreased with increasing erythrocyte composition of total n-3 fatty acids and rose with increasing erythrocyte composition of total n-6 fatty acids. However, these findings were noted only among non-users of NSAIDs and not among NSAID users. No relationship was observed between any of the n-6 or n-3 fatty acids measures |
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The omega-6 and omega-3 polyunsaturated fatty acids and modifiable breast cancer risk factors. $108 Experimental evidence suggests that omega-6 (n-6) fatty acids have mammary tumor promoting effects whereas omega-3 (n-3) fatty acids inhibit tumor growth. These two families of fatty acids may influence breast cancer development by impacting prostaglandin E2 (PGE2) formation and consequently estradiol synthesis. Whether this effect on estrogen production can be observed in the circulation or in breast tissue, as reflected on a mammogram, is unknown. Therefore, using fatty acids in erythrocytes as a biomarker of recent dietary intake, we sought to establish the relationship between the n-6 and n-3 fatty acids with both serum estradiol and mammographic breast density, two well-established modifiable breast cancer risk factors. We hypothesized that n-6 fatty acids are positively related and n-3 fatty acids negatively related to both risk factors. Nonsteroidal anti-inflammatory drugs (NSAIDs) also inhibit PGE2 formation, therefore we further hypothesized that estradiol levels would be lower among NSAID users. NSAID data was not available at the time of mammogram; hence the relationship between NSAID use and mammographic density could not accurately be assessed. To test our hypotheses we conducted several investigations ancillary to the Mammograms and Masses Study (MAMS), a case control study of the determinants of mammographic breast density. Participants were eligible for this compilation of studies if they were breast cancer-free, postmenopausal and not taking exogenous hormones. We observed significantly lower levels of serum estradiol among current users of NSAIDs as compared to non-users of NSAIDs. Further, as hypothesized, estradiol concentration decreased with increasing erythrocyte composition of total n-3 fatty acids and rose with increasing erythrocyte composition of total n-6 fatty acids. However, these findings were noted only among non-users of NSAIDs and not among NSAID users. No relationship was observed between any of the n-6 or n-3 fatty acids measures |
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The omega-6 and omega-3 polyunsaturated fatty acids and modifiable breast cancer risk factors. $49.99 Experimental evidence suggests that omega-6 (n-6) fatty acids have mammary tumor promoting effects whereas omega-3 (n-3) fatty acids inhibit tumor growth. These two families of fatty acids may influence breast cancer development by impacting prostaglandin E2 (PGE2) formation and consequently estradiol synthesis. Whether this effect on estrogen production can be observed in the circulation or in breast tissue, as reflected on a mammogram, is unknown. Therefore, using fatty acids in erythrocytes as a biomarker of recent dietary intake, we sought to establish the relationship between the n-6 and n-3 fatty acids with both serum estradiol and mammographic breast density, two well-established modifiable breast cancer risk factors. We hypothesized that n-6 fatty acids are positively related and n-3 fatty acids negatively related to both risk factors. Nonsteroidal anti-inflammatory drugs (NSAIDs) also inhibit PGE2 formation, therefore we further hypothesized that estradiol levels would be lower among NSAID users. NSAID data was not available at the time of mammogram; hence the relationship between NSAID use and mammographic density could not accurately be assessed. To test our hypotheses we conducted several investigations ancillary to the Mammograms and Masses Study (MAMS), a case control study of the determinants of mammographic breast density. Participants were eligible for this compilation of studies if they were breast cancer-free, postmenopausal and not taking exogenous hormones. We observed significantly lower levels of serum estradiol among current users of NSAIDs as compared to non-users of NSAIDs. Further, as hypothesized, estradiol concentration decreased with increasing erythrocyte composition of total n-3 fatty acids and rose with increasing erythrocyte composition of total n-6 fatty acids. However, these findings were noted only among non-users of NSAIDs and not among NSAID users. No relationship was observed between any of the n-6 or n-3 fatty acids measures |
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The role of beta3 integrin and its associating molecules in bone biology and bone metastasis. $49.99 The focus of this dissertation has been to understand the role of beta3 integrin and its associating molecules CD47 and thrombospondin-1 (TSP1) in bone biology and bone metastasis. We have previously shown that platelet and osteoclast beta3 integrins are critical for bone metastasis. In the first part of this thesis, we studied the effect of pharmacological targeting of molecules that activate platelet alphaIIbbeta3 on bone metastasis. Metastatic tumor cells can produce alphaIIbbeta3 activators, such as ADP and thromboxane A2 (TXA2). Inhibitors of alphaIIbbeta3 decrease bone metastases in mice but are associated with significant bleeding. We examined the role of a novel ADPase, APT102, and an inhibitor of TXA2 synthesis, acetylsalicylic acid (aspirin/ASA), in mouse models of bone metastases. We found that treatment with ASA and APT102 in combination (ASA+APT102) significantly decreased breast cancer and melanoma bone metastases in mice with fewer bleeding complications than observed with alphaIIbbeta3 inhibition. We conclude that blocking molecules that activate alphaIIbbeta3 is an efficient and safe approach for treating bone metastasis. In the second part of this thesis, we examined the role of CD47 and TSP1, molecules previously shown to augment alphaIIbbeta3 function, in osteoclasts and bone metastasis. We hypothesized that TSP1 and CD47 will also augment alphavbeta3 function in osteoclasts and affect bone metastasis. We observed that TSP1-/- mice have increased bone mineral density and decreased serum CTX levels compared to WT controls, consistent with an osteoclast defect. Osteoclast defects are associated with decreased bone tumor burden. However, bone tumor burden was not decreased in TSP1-/- mice after intra-cardiac delivery of tumor cells. Notably, loss of TSP1 is reported to enhance angiogenesis through an interaction with CD36, not CD47, which could explain these unexpected results. Thus, we evaluated osteoclastogenesis and bone metastasis in CD47-/- |
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The role of beta3 integrin and its associating molecules in bone biology and bone metastasis. $49.99 The focus of this dissertation has been to understand the role of beta3 integrin and its associating molecules CD47 and thrombospondin-1 (TSP1) in bone biology and bone metastasis. We have previously shown that platelet and osteoclast beta3 integrins are critical for bone metastasis. In the first part of this thesis, we studied the effect of pharmacological targeting of molecules that activate platelet alphaIIbbeta3 on bone metastasis. Metastatic tumor cells can produce alphaIIbbeta3 activators, such as ADP and thromboxane A2 (TXA2). Inhibitors of alphaIIbbeta3 decrease bone metastases in mice but are associated with significant bleeding. We examined the role of a novel ADPase, APT102, and an inhibitor of TXA2 synthesis, acetylsalicylic acid (aspirin/ASA), in mouse models of bone metastases. We found that treatment with ASA and APT102 in combination (ASA+APT102) significantly decreased breast cancer and melanoma bone metastases in mice with fewer bleeding complications than observed with alphaIIbbeta3 inhibition. We conclude that blocking molecules that activate alphaIIbbeta3 is an efficient and safe approach for treating bone metastasis. In the second part of this thesis, we examined the role of CD47 and TSP1, molecules previously shown to augment alphaIIbbeta3 function, in osteoclasts and bone metastasis. We hypothesized that TSP1 and CD47 will also augment alphavbeta3 function in osteoclasts and affect bone metastasis. We observed that TSP1-/- mice have increased bone mineral density and decreased serum CTX levels compared to WT controls, consistent with an osteoclast defect. Osteoclast defects are associated with decreased bone tumor burden. However, bone tumor burden was not decreased in TSP1-/- mice after intra-cardiac delivery of tumor cells. Notably, loss of TSP1 is reported to enhance angiogenesis through an interaction with CD36, not CD47, which could explain these unexpected results. Thus, we evaluated osteoclastogenesis and bone metastasis in CD47-/- |