Fish consumption and breast cancer risk: An ecological study

Kaizer, Leonard; Boyd, Norman F.; Kriukov, Valentina; Tritchler, David

doi:10.1080/01635588909514002

Cited by 202 publications

(94 citation statements)

References 24 publications

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“…Conversely, diets rich in n-3 FAs, such as a-linolenic (18:3, LNA), eicosapentaenoic (20:5, EPA) and docosahexaenoic (22:6, DHA) acids, reduced the incidence, growth and metastasis of both induced and transplanted rat mammary tumours (Pritchard et al, 1989;Cave, 1991). These results could explain the increasing incidence of breast cancer in the USA, where LA-rich vegetable oil consumption has steadily increased, as well as the lower incidence in countries where fish oils (rich in n-3 FAs) constitute a higher proportion of the dietary lipid intake (Carroll & Hopkins, 1979;Kaizer et al, 1989).…”

mentioning

confidence: 74%

n-3 and n-6 fatty acid processing and growth effects in neoplastic and non-cancerous human mammary epithelial cell lines

Grammatikos¹,

Subbaiah²,

Victor³

et al. 1994

Br J Cancer

144

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The type rather than the amount of dietary fat may be more important in breast carcinogenesis. While animal studies support this view, little is known about the effects of essential fatty acids (EFAs) at the cellular level. The MCF-7 breast cancer and the MCF-10A non-cancerous human mammary epithelial cell lines are compared in terms of growth response to EFAs and ability to incorporate and process the EFAs. Eicosapentaenoic (EPA, n-3) and docosahexaenoic (DHA, n-3) acids, presented bound to albumin, inhibited the growth of MCF-7 cells by as much as 50% in a dose-dependent manner (6-30 microM) in medium containing 0.5% serum. alpha-Linolenic (LNA, n-3) and arachidonic (AA, n-6) acids inhibited growth less extensively, while linoleic acid (LA, n-6) had no effect. In contrast, MCF-10A cells were not inhibited by any of the EFAs at levels below 24 microM. The differential effects of AA, EPA and DHA on MCF-7 and MCF-10A cells support a protective role of highly unsaturated essential fatty acids against breast cancer. The EFAs were primarily incorporated into phosphoglycerides. MCF-7 cells showed chain elongations and possibly delta 8 desaturation, but no AA was formed from LA, nor EPA or DHA from LNA. In contrast, MCF-10A cells desaturated and elongated the exogenous EFAs via all the known pathways. These findings suggest defects in the desaturating enzymes of MCF-7 cells. LNA, DHA and AA presented to MCF-7 cells in phospholipid liposomes inhibited growth as extensively as albumin-bound free acids, but were less extensively incorporated, suggesting different mechanisms of inhibition for the two methods.

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mentioning

confidence: 74%

n-3 and n-6 fatty acid processing and growth effects in neoplastic and non-cancerous human mammary epithelial cell lines

Grammatikos¹,

Subbaiah²,

Victor³

et al. 1994

Br J Cancer

144

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“…In contrast, n-3 PUFAs have frequently been shown to inhibit tumour development in experimental studies (Karmali et al, 1984;O'Connor et al, 1989;de Bravo et al, 1991;Mtehle et al, 1995). This has been supported in a human study on fish diet (rich in n-3 PUFAs) and breast cancer rates (Kaizer et al, 1989). In vitro, the inhibitory effect of PUFAs on cell proliferation has been well documented (Morisaki et al, 1982;Begin et al, 1986;Rose and Connolly, 1991;H0stmark and Lystad, 1992;Krokan et al, 1993;Mzehle et al, 1995).…”

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confidence: 83%

Differential effect of polyunsaturated fatty acids on cell proliferation during human epithelial in vitro carcinogenesis: involvement of epidermal growth factor receptor tyrosine kinase

Mollerup

Haugen²

1996

Br J Cancer

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Summary Polyunsaturated fatty acids (PUFAs) have been implicated in tumour development and have been shown to influence cell proliferation in vitro. We report here that n-3 and n-6 PUFAs at concentration > 10 gM inhibited the proliferation of a human kidney epithelial cell line (2IHKE), which has retained phenotypic characteristics of normal kidney epithelial cells. In contrast, the proliferation was stimulated by n-3 and n-6 PUFAs at concentrations <10 gM under defined growth conditions. The stimulatory effect of n-3 and n-6 PUFAs was even more profound in the presence of EGF. In human kidney epithelial cell lines reflecting different stages of transformation (1IHKE and ITHKEras), the stimulatory effect was abrogated both in the presence and absence of EGF. Saturated fatty acids did not show any stimulatory effect on cell growth. The tyrosine kinase inhibitors genistein and tyrphostin-47 inhibited EGF-induced protein tyrosine phosphorylation dose-dependently in the 2IHKE cells, and abolished the growth stimulatory effect of docosahexaenoic acid (DHA). This indicates the involvement of EGF receptor tyrosine kinase activity in the observed increase in cell proliferation.

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“…Previous reports from our laboratory have extensively described the anticancer activities of DHA in various in vitro cell systems as well as in vivo models. 4,5,14,32,33,35,42 Furthermore, our laboratory has reported the added benefit of either using DHA in conjunction with known anticancer compounds or directly conjugating DHA with compounds to significantly enhance its anticancer efficacy. Since DHA is the most abundant PUFA in the brain and has been shown to possess anticancer properties, we hypothesized that combining DHA with a currently used chemotherapeutic reagent would result in significantly greater anticancer potential.…”

Section: Discussionmentioning

confidence: 99%

Enhanced anticancer properties of lomustine in conjunction with docosahexaenoic acid in glioblastoma cell lines

Harvey

Saaddatzadeh

et al. 2015

JNS

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abbreviatioNs BCA = bicinchoninic acid; CSC = Cell Systems Corporation; DHA = docosahexaenoic acid; DMEM = Dulbecco's modified essential medium; DPA = docosapentaenoic acid; ED 50 = median effective dose; EMEM = Eagle's minimum essential medium; EPA = eicosapentaenoic acid; FBS = fetal bovine serum; HBMEC = human brain microvascular endothelial cell; HCCMEC = human cerebral cortex microvascular endothelial cell; OD = optical density; PARP = poly (ADP-ribose) polymerase; PBS = phosphate-buffered saline; PUFA = polyunsaturated fatty acid. obJect Glioblastoma is a rapidly infiltrating tumor that consistently rematerializes despite various forms of aggressive treatment. Brain tumors are commonly treated with alkylating drugs, such as lomustine, which are chemotherapeutic agents. Use of these drugs, however, is associated with serious side effects. To reduce the side effects, one approach is to combine lower doses of chemotherapeutic drugs with other nontoxic anticancer agents. In this study, using glioblastoma cell lines, the authors investigated the anticancer effects of lomustine, alone and in combination with docosahexaenoic acid (DHA), an omega-3 polyunsaturated fatty acid normally abundant in the brain and known for its anticancer potential. methods Cells were cultured from 3 human-derived tumor cell lines (U87-MG, DB029, and MHBT161) and supplemented with either DHA or lomustine to determine the growth inhibitory potential using WST-1, a mitochondrial functional indicator. Human-derived cerebral cortex microvascular endothelial cells served as a normal phenotypic control. Cellular incorporation of DHA was analyzed by gas chromatography. Using flow cytometric analysis, the DHA and/or lomustine effect on induction of apoptosis and/or necrosis was quantified; subsequently, the DHA and lomustine effect on cell cycle progression was also assessed. Western blot analysis confirmed the role of downstream cellular targets. results U87-MG growth was inhibited with the supplementation of either DHA (ED 50 68.3 mM) or lomustine (ED 50 68.1 mM); however, growth inhibition was enhanced when U87-MG cells were administered equimolar doses of each compound, resulting in nearly total growth inhibition at 50 mM. Gas chromatography analysis of the fatty acid profile in DHA-supplemented U87-MG cells resulted in a linear dose-dependent increase in DHA incorporation (< 60 mM). The combination of DHA and lomustine potently induced U87-MG apoptosis and necrosis as indicated by flow cytometric analysis. Activation of caspase-3 and poly (ADP-ribose) polymerase (PARP) was evident in lomustine-treated U87-MG cells, although this activation did not appear to be dependent on DHA supplementation. Additionally, lomustine-treated cells' growth arrested in the G 2 /M cell cycle stage, regardless of the presence of DHA. Similar to the U87-MG observations, the combination of DHA and lomustine resulted in growth inhibition of 2 additional human-derived glioblastoma cell lines, DB029 and MHBT161. Importantly, in primary human-derived cerebral corte...

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Fish consumption and breast cancer risk: An ecological study

Cited by 202 publications

References 24 publications

n-3 and n-6 fatty acid processing and growth effects in neoplastic and non-cancerous human mammary epithelial cell lines

n-3 and n-6 fatty acid processing and growth effects in neoplastic and non-cancerous human mammary epithelial cell lines

Differential effect of polyunsaturated fatty acids on cell proliferation during human epithelial in vitro carcinogenesis: involvement of epidermal growth factor receptor tyrosine kinase

Enhanced anticancer properties of lomustine in conjunction with docosahexaenoic acid in glioblastoma cell lines

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