Receptor to slow breast cancer metastasis identified
https://www.sciencedaily.com/releases/2016/10/161003121008.htm
By therapeutically targeting the receptor for advanced glycation end-products (RAGE) in breast cancer cells, researchers decreased tumor growth, reduced tumor angiogenesis and recruitment of inflammatory cells, and dramatically decreased metastasis to the lung and the liver.
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Not a Komen fan but I like that they are paying more attention to mets research.
Comments
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Dietary changes could be of value, too, in reducing the formation of advanced glycation products (AGE's)
Advanced Glycation End Products in Foods and a Practical Guide to Their Reduction in the Diet
"dry heat promotes new dAGE formation by >10- to 100-fold above the uncooked state across food categories. Animal-derived foods that are high in fat and protein are generally AGE-rich and prone to new AGE formation during cooking. In contrast, carbohydrate-rich foods such as vegetables, fruits, whole grains, and milk contain relatively few AGEs, even after cooking. The formation of new dAGEs during cooking was prevented by the AGE inhibitory compound aminoguanidine and significantly reduced by cooking with moist heat, using shorter cooking times, cooking at lower temperatures, and by use of acidic ingredients such as lemon juice or vinegar. The new dAGE database provides a valuable instrument for estimating dAGE intake and for guiding food choices to reduce dAGE intake."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3704564/
(Uribarri, 2010)
Dietary factors and low-grade inflammation in relation to overweight and obesity.
"Healthy eating patterns are associated with lower circulating concentrations of inflammatory markers. Among the components of a healthy diet, whole grains, vegetables and fruits, and fish are all associated with lower inflammation. AGE are associated with enhanced oxidative stress and inflammation. SFA and trans-MUFA are pro-inflammatory, while PUFA, especially long-chain n-3 PUFA, are anti-inflammatory. Hyperglycaemia induces both postprandial and chronic low-grade inflammation. Vitamin C, vitamin E and carotenoids decrease the circulating concentrations of inflammatory markers."
http://www.ncbi.nlm.nih.gov/pubmed/22133051
(Cader, 2011)
Quercetin protects necrotic insult and promotes apoptosis by attenuating the expression of RAGE and its ligand HMGB1 in human breast adenocarcinoma cells.
"The accumulation of RAGE and its ligand high-mobility group box proteins-1 (HMGB1) activates complex signaling network for cell survival and evades apoptosis. Therefore, targeting the RAGE-mediated signaling could be the promising strategies for the therapeutic potential of cancer. This study was aimed to examine the biological potential of quercetin on the regulation of RAGE- and HMGB1-mediated activation of NF-κB and induction of apoptotic cell death in MCF-7 cells.
http://www.ncbi.nlm.nih.gov/pubmed/25983116(Dhumale SS, 2015)
Dietary Advanced Glycation End Products and Risk Factors for Chronic Disease: A Systematic Review of Randomised Controlled Trials.
" A high AGE diet increased circulating tumour necrosis factor-alpha and AGEs in all populations. A high AGE diet increased 8-isoprostanes in healthy adults, and vascular cell adhesion molecule-1 (VCAM-1) in patients with diabetes. Markers of CKD were not widely assessed. The evidence presented indicates that a high AGE diet may contribute to risk factors associated with chronic disease, such as inflammation and oxidative stress, however, due to a lack of high quality randomised trials, more research is required."
http://www.ncbi.nlm.nih.gov/pubmed/26938557
(Clarke, 2016)
Serum Levels of Toxic AGEs (TAGE) May Be a Promising Novel Biomarker for the Onset/Progression of Lifestyle-Related Diseases.
http://www.ncbi.nlm.nih.gov/pubmed/2733848
(Takeuchi, 2016)
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Thanks, Falleaves! Interesting about quercetin. Capers are supposed to be very rich in quercetin.
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Heidihill - "Capers are supposed to be very rich in quercetin" may be the best news I've had all month! I LOVE capers and use them generously. Now I can justify them as a "health food."
Thank you!
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Plus, quercetin appears to be good for bone health, too! (So, bring on the capers!)
Dietary quercetin inhibits bone loss without effect on the uterus in ovariectomized mice.
Quercetin is a major dietary flavonoid found in onions and other vegetables, and potentially has beneficial effects on disease prevention. In the present study, we demonstrate for the first time the effects of dietary quercetin on bone loss and uterine weight loss by ovariectomy in vivo. Female mice were ovariectomized (OVX) and were randomly allocated to 3 groups: a control diet or a diet with 0.25% (LQ) or 2.5% quercetin (HQ). After 4 weeks, dietary quercetin had no effects on uterine weight in OVX mice, but bone mineral density of the lumbar spine L4 and femur measured by peripheral quantitative computed tomography (pQCT) was higher in both the sham and the HQ groups than in the OVX group. Histomorphometric analysis showed that the HQ group restored bone volume (BV/TV) completely in distal femoral cancellous bone, but did not reduce the osteoclast surface area and osteoclast number when compared with the OVX group. In in-vitro experiments using mouse monocyte/macrophage cell line RAW264.7 cells, however, quercetin and its conjugate, quercetin-3-O-beta-D: -glucuronide dose-dependently inhibited the receptor activator of nuclear factor-kappa B ligand (RANKL)-induced osteoclast differentiation, and the RANKL-stimulated expression of osteoclast related genes was also inhibited by quercetin. The luciferase reporter assay showed that quercetin did not appear to have estrogenic activity through estrogen receptors. These results suggest that dietary quercetin inhibits bone loss without effect on the uterus in OVX mice and does not act as a potent inhibitor of osteoclastogenesis or as a selective estrogen receptor modulator in vivo.
http://www.ncbi.nlm.nih.gov/pubmed/19495926
(Tsuji, 2009)
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