Lani
06-25-2014, 02:31 PM
erolemia induces angiogenesis & accelerates growth of breast tumors in mice
(nonher2+ breast tumors) If you want to wait until the experiment is done with her2+ bc cells, there is still time to indulge. BC cells use more cholesterol to make cell membranes than normal cells (as they grow faster) and her2+ bc has already been shown to be sensitive to some inibitors of fatty acid synthesis.
So a betting person would figure out that high cholesterol foods are bad for the cardiovascular system, that CV disease kills more women than breast cancer, if a woman already has been treated for breast cancer with drugs/radiation which take a toll on the cardiovascular system as well, and it wouldn't be unlikely that cutting down on cholesterol might be beneficial for a number of reasons
Am J Pathol. 2014 Jul;184(7):2099-110. doi: 10.1016/j.ajpath.2014.03.006.
Hypercholesterolemia Induces Angiogenesis and Accelerates Growth of Breast Tumors in Vivo.
Pelton K1, Coticchia CM2, Curatolo AS3, Schaffner CP4, Zurakowski D5, Solomon KR6, Moses MA2.
Author information
Abstract
Obesity and metabolic syndrome are linked to an increased prevalence of breast cancer among postmenopausal women. A common feature of obesity, metabolic syndrome, and a Western diet rich in saturated fat is a high level of circulating cholesterol. Epidemiological reports investigating the relationship between high circulating cholesterol levels, cholesterol-lowering drugs, and breast cancer are conflicting. Here, we modeled this complex condition in a well-controlled, preclinical animal model using innovative isocaloric diets. Female severe combined immunodeficient mice were fed a low-fat/no-cholesterol diet and then randomized to four isocaloric diet groups: low-fat/no-cholesterol diet, with or without ezetimibe (cholesterol-lowering drug), and high-fat/high-cholesterol diet, with or without ezetimibe. Mice were implanted orthotopically with MDA-MB-231 cells. Breast tumors from animals fed the high-fat/high-cholesterol diet exhibited the fastest progression. Significant differences in serum cholesterol level between groups were achieved and maintained throughout the study; however, no differences were observed in intratumoral cholesterol levels. To determine the mechanism of cholesterol-induced tumor progression, we analyzed tumor proliferation, apoptosis, and angiogenesis and found a significantly greater percentage of proliferating cells from mice fed the high-fat/high-cholesterol diet. Tumors from hypercholesterolemic animals displayed significantly less apoptosis compared with the other groups. Tumors from high-fat/high-cholesterol mice had significantly higher microvessel density compared with tumors from the other groups. These results demonstrate that hypercholesterolemia induces angiogenesis and accelerates breast tumor growth in vivo.
Copyright © 2014 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.
PMID: 24952430 [
(nonher2+ breast tumors) If you want to wait until the experiment is done with her2+ bc cells, there is still time to indulge. BC cells use more cholesterol to make cell membranes than normal cells (as they grow faster) and her2+ bc has already been shown to be sensitive to some inibitors of fatty acid synthesis.
So a betting person would figure out that high cholesterol foods are bad for the cardiovascular system, that CV disease kills more women than breast cancer, if a woman already has been treated for breast cancer with drugs/radiation which take a toll on the cardiovascular system as well, and it wouldn't be unlikely that cutting down on cholesterol might be beneficial for a number of reasons
Am J Pathol. 2014 Jul;184(7):2099-110. doi: 10.1016/j.ajpath.2014.03.006.
Hypercholesterolemia Induces Angiogenesis and Accelerates Growth of Breast Tumors in Vivo.
Pelton K1, Coticchia CM2, Curatolo AS3, Schaffner CP4, Zurakowski D5, Solomon KR6, Moses MA2.
Author information
Abstract
Obesity and metabolic syndrome are linked to an increased prevalence of breast cancer among postmenopausal women. A common feature of obesity, metabolic syndrome, and a Western diet rich in saturated fat is a high level of circulating cholesterol. Epidemiological reports investigating the relationship between high circulating cholesterol levels, cholesterol-lowering drugs, and breast cancer are conflicting. Here, we modeled this complex condition in a well-controlled, preclinical animal model using innovative isocaloric diets. Female severe combined immunodeficient mice were fed a low-fat/no-cholesterol diet and then randomized to four isocaloric diet groups: low-fat/no-cholesterol diet, with or without ezetimibe (cholesterol-lowering drug), and high-fat/high-cholesterol diet, with or without ezetimibe. Mice were implanted orthotopically with MDA-MB-231 cells. Breast tumors from animals fed the high-fat/high-cholesterol diet exhibited the fastest progression. Significant differences in serum cholesterol level between groups were achieved and maintained throughout the study; however, no differences were observed in intratumoral cholesterol levels. To determine the mechanism of cholesterol-induced tumor progression, we analyzed tumor proliferation, apoptosis, and angiogenesis and found a significantly greater percentage of proliferating cells from mice fed the high-fat/high-cholesterol diet. Tumors from hypercholesterolemic animals displayed significantly less apoptosis compared with the other groups. Tumors from high-fat/high-cholesterol mice had significantly higher microvessel density compared with tumors from the other groups. These results demonstrate that hypercholesterolemia induces angiogenesis and accelerates breast tumor growth in vivo.
Copyright © 2014 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.
PMID: 24952430 [