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Increased dietary levels of [alpha]-linoleic acid inhibit mammary tumor growth and metastasis
Objective The aim of this study was to determine whether [alpha]-linolenic acid (ALA [omega]-3 fatty acid) enriched diet affects growth parameters when applied to a syngeneic model of mammary carcinoma. Materials and methods BALB/c mice were divided and fed with: 1) a chia oil diet, rich in ALA or 2...
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Published in: | European journal of nutrition 2017-03, Vol.56 (2), p.509 |
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creator | Vara-messler, Marianela Pasqualini, Maria E Comba, Andrea Silva, Renata Buccellati, Carola Trenti, Annalisa Trevisi, Lucia Eynard, Aldo R Sala, Angelo Bolego, Chiara Valentich, Mirta A |
description | Objective The aim of this study was to determine whether [alpha]-linolenic acid (ALA [omega]-3 fatty acid) enriched diet affects growth parameters when applied to a syngeneic model of mammary carcinoma. Materials and methods BALB/c mice were divided and fed with: 1) a chia oil diet, rich in ALA or 2) a corn oil diet, rich in linoleic acid (LA [omega]-6 fatty acid). Mice were subcutaneously inoculated with a tumor cell line LM3, derived from a murine mammary adenocarcinoma. Results After 35 days, tumor incidence, weight, volume and metastasis number were lower in the ALA-fed mice, while tumor latency time was higher, and the release of pro-tumor metabolites derived from [omega]-6 fatty acids decreased in the tumor. Compared to the control group, a lower number of mitosis, a higher number of apoptotic bodies and higher T-lymphocyte infiltration were consistently observed in the ALA group. An ALA-rich diet decreased the estrogen receptor (ER) [alpha] expression, a recognized breast cancer promotor while showing an opposite effect on ER[beta] in tumor lysates. Conclusion These data support the anticancer effect of an ALA-enriched diet, which might be used as a dietary strategy in breast cancer prevention. |
doi_str_mv | 10.1007/s00394-015-1096-6 |
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Materials and methods BALB/c mice were divided and fed with: 1) a chia oil diet, rich in ALA or 2) a corn oil diet, rich in linoleic acid (LA [omega]-6 fatty acid). Mice were subcutaneously inoculated with a tumor cell line LM3, derived from a murine mammary adenocarcinoma. Results After 35 days, tumor incidence, weight, volume and metastasis number were lower in the ALA-fed mice, while tumor latency time was higher, and the release of pro-tumor metabolites derived from [omega]-6 fatty acids decreased in the tumor. Compared to the control group, a lower number of mitosis, a higher number of apoptotic bodies and higher T-lymphocyte infiltration were consistently observed in the ALA group. An ALA-rich diet decreased the estrogen receptor (ER) [alpha] expression, a recognized breast cancer promotor while showing an opposite effect on ER[beta] in tumor lysates. 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Materials and methods BALB/c mice were divided and fed with: 1) a chia oil diet, rich in ALA or 2) a corn oil diet, rich in linoleic acid (LA [omega]-6 fatty acid). Mice were subcutaneously inoculated with a tumor cell line LM3, derived from a murine mammary adenocarcinoma. Results After 35 days, tumor incidence, weight, volume and metastasis number were lower in the ALA-fed mice, while tumor latency time was higher, and the release of pro-tumor metabolites derived from [omega]-6 fatty acids decreased in the tumor. Compared to the control group, a lower number of mitosis, a higher number of apoptotic bodies and higher T-lymphocyte infiltration were consistently observed in the ALA group. An ALA-rich diet decreased the estrogen receptor (ER) [alpha] expression, a recognized breast cancer promotor while showing an opposite effect on ER[beta] in tumor lysates. 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Materials and methods BALB/c mice were divided and fed with: 1) a chia oil diet, rich in ALA or 2) a corn oil diet, rich in linoleic acid (LA [omega]-6 fatty acid). Mice were subcutaneously inoculated with a tumor cell line LM3, derived from a murine mammary adenocarcinoma. Results After 35 days, tumor incidence, weight, volume and metastasis number were lower in the ALA-fed mice, while tumor latency time was higher, and the release of pro-tumor metabolites derived from [omega]-6 fatty acids decreased in the tumor. Compared to the control group, a lower number of mitosis, a higher number of apoptotic bodies and higher T-lymphocyte infiltration were consistently observed in the ALA group. An ALA-rich diet decreased the estrogen receptor (ER) [alpha] expression, a recognized breast cancer promotor while showing an opposite effect on ER[beta] in tumor lysates. 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title | Increased dietary levels of [alpha]-linoleic acid inhibit mammary tumor growth and metastasis |
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