Consumption of omega‐3 fatty acids and the risk of skin cancers: A systematic review and meta‐analysis

Noël, Sophie; Stoneham, Adam C.S.; Olsen, Catherine M.; Rhodes, Lesley E.; Green, Adèle C.

doi:10.1002/ijc.28630

Cited by 44 publications

(32 citation statements)

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“…These n‐3 and n‐6 fatty acids reduce tumor growth by inhibiting cell growth, apoptosis, angiogenesis and inflammation . Observational studies have discovered that higher levels of dietary n‐3 fatty acid intake are inversely associated with melanoma risk . A hospital‐based case–control study conducted in Italy showed that weekly consumption of fatty fish that was rich in n‐3 fatty acids was associated with a reduced risk of melanoma (odds ratio [OR] = 0.52, 95% confidence interval [CI] = 0.34–0.78).…”

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confidence: 99%

Polyunsaturated fatty acids and risk of melanoma: A Mendelian randomisation analysis

Liyanage

Law

Ong

et al. 2018

Intl Journal of Cancer

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Melanoma is the deadliest form of skin cancer, mainly affecting populations of European ancestry. Some observational studies suggest that particular diets reduce melanoma risk, putatively through an increase in polyunsaturated fatty acid (PUFA) consumption. However, interpretation of these observational findings is difficult due to residual confounding or reverse causality. To date, a randomized controlled trial has not been carried out to examine the relationship between PUFAs and melanoma. Hence, we performed a Mendelian randomisation (MR) study to evaluate the link between PUFAs and melanoma. To perform MR, we used summary results from the largest risk genome-wide association study (GWAS) meta-analysis of melanoma, consisting of 12,874 cases and 23,203 controls. As instrumental variables we selected SNPs associated with PUFA levels from a GWAS meta-analysis of PUFA levels, from the CHARGE consortium. We used the inverse variance weighted method to estimate a causal odds ratio. To aid interpretation, we established a benchmark "large" predicted change in PUFAs in which, for example, an increase in docosahexaenoic acid (DPA) of 0.17 units (equal to 1 standard deviation) moves a person from the 17 percentile to the median. Raising PUFA levels by a large amount (increasing DPA by 0.17 units) only negligibly changed melanoma risk: odds ratio [OR] = 1.03 (95% confidence interval [CI] = 0.96-1.10). Other PUFAs yielded similar results as DPA. Our MR analysis suggests that the effect of PUFA levels on melanoma risk is either zero or very small.

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confidence: 99%

Polyunsaturated fatty acids and risk of melanoma: A Mendelian randomisation analysis

Liyanage

Law

Ong

et al. 2018

Intl Journal of Cancer

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“…Epidemiological studies regarding the association between intake or plasma concentrations of n-3 PUFAs and cancer risk reduction, provide limited and sometime contrasting data (Dahm et al, 2012;Zheng et al, 2013;Crowe et al, 2014;Noel et al, 2014). Nevertheless, in a meta-analysis and systematic review of prospective cohort studies, dietary intake of fish derived n-3 PUFAs, such as DHA and EPA, but not shorter alpha linolenic acid (ALA), was associated with a lower risk of breast cancer (Zheng et al, 2013).…”

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Effect of Docosahexaenoic Acid on Cell Cycle Pathways in Breast Cell Lines With Different Transformation Degree

Rescigno

Capasso

Tecce

2015

Journal Cellular Physiology

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n-3 polyunsaturated fatty acids (PUFAs), such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), abundant in fish, have been shown to affect development and progression of some types of cancer, including breast cancer. The aim of our study was to further analyze and clarify the effects of these nutrients on the molecular mechanisms underlying breast cancer. Following treatments with DHA we examined cell viability, death, cell cycle, and some molecular effects in breast cell lines with different transformation, phenotypic, and biochemical characteristics (MCF-10A, MCF-7, SK-BR-3, ZR-75-1). These investigations showed that DHA is able to affect cell viability, proliferation, and cell cycle progression in a different way in each assayed breast cell line. The activation of ERK1/2 and STAT3 pathways and the expression and/or activation of molecules involved in cell cycle regulation such as p21(Waf1/Cip1) and p53, are very differently regulated by DHA treatments in each cell model. DHA selectively: (i) arrests non tumoral MCF-10A breast cells in G0 /G1 cycle phase, activating p21(Waf1/Cip1) , and p53, (ii) induces to death highly transformed breast cells SK-BR-3, reducing ERK1/2 and STAT3 phosphorylation and (iii) only slightly affects each analyzed process in MCF-7 breast cell line with transformation degree lower than SK-BR-3 cells. These findings suggest a more relevant inhibitory role of DHA within early development and late progression of breast cancer cell transformation and a variable effect in the other phases, depending on individual molecular properties and degree of malignancy of each clinical case.

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“…Recently, a review and meta-analysis was conducted to determine the relationship between skin cancer and dietary omega-3 intake [18]. While the data were limited, the investigators reported that intake of high omega-3 was inversely associated with melanoma (only one estimate) and SCC, although the latter was not significant.…”

Section: Baumann and Ruschmentioning

confidence: 99%

Role of Dietary Fat in Ultraviolet Light–Induced Carcinogenic Expression

Black¹

2014

J Integr Oncol

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EditorialThe indictment of fat as a dietary constituent that potentiates carcinogenesis arose from a study of Watson and Mellanby in 1930 [1]. Animal diets containing high levels of butterfat (12.5-25%) were shown to enhance coal tar-induced skin tumor formation. After this seminal observation, intense investigations of the effects of dietary fat on chemically-induced carcinogenesis were conducted during the 1930s through the 1950s. There were several conclusions from these studies that are noteworthy [2]. These, however, must be tempered by the fact that many of these early studies failed to control for major dietary parameters, e.g., caloric density. And although much of the exacerbation of fat on tumor formation reported in these early studies could be explained on the basis of increased caloric intake, fat, per se, increased the rate of tumor formation, particularly when total caloric intake was restricted. Also, much of the exacerbation by fat on tumor formation occurred during the post initiation stage of carcinogenesis. Baumann and Rusch [3] first demonstrated that dietary fat also had an influence on ultraviolet light (UVL) induced carcinogenesis. These investigators employed a high-fat diet that contained up to 30% hydrogenated cottonseed oil. This resulted in a four week shorter tumor latent period than that which occurred in low-fat controls. However, this line of investigation ended with the advent of World War II and was not resumed for nearly 45 years. This was unfortunate as UVL-carcinogenesis is the main etiologic agent in skin carcinogenesis. Nearly 90% of all human skin cancers are the result of solar UVL [4]. Thus, studies of skin carcinogenesis employing UVL are the most relevant to the clinical condition. There are other advantages to employing a physical carcinogenic agent over chemical carcinogens in dietary studies. UVL involves no activation/detoxification of the presumed carcinogenic species; no competitive chemical inhibition; no binding to target molecules; and no transport to respective target sites. Changing the cells chemical milieu through dietary modification could have an impact on any of these activities affecting chemical carcinogenesis. UVL allows investigation of the direct underlying mechanisms of dietary modification of the skin cancerization process.Dietary lipid was further implicated in cancer when Denham Harmon [5] developed the Free Radical Theory of disease. Cognizant of the vulnerability of polyunsaturated fatty acids to free radical attack, he recommended that dietary levels of PUFA be reduced in order to reduce cancer risk [6]. Indeed, the first report on diet and UVL carcinogenesis following the seminal observation in 1939, appeared to be in agreement with Harman's recommendation. Mice were fed semidefined, isocaloric diets containing 0.75 to 4.0 % (w/w) omega-6 fatty acid (Corn oil), and subjected to a UVL regimen. The tumor latent period was dramatically lengthened and tumor multiplicity reduced as the dietary PUFA level was reduced [7].These tumor parameters ...

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Consumption of omega‐3 fatty acids and the risk of skin cancers: A systematic review and meta‐analysis

Cited by 44 publications

References 44 publications

Polyunsaturated fatty acids and risk of melanoma: A Mendelian randomisation analysis

Polyunsaturated fatty acids and risk of melanoma: A Mendelian randomisation analysis

Effect of Docosahexaenoic Acid on Cell Cycle Pathways in Breast Cell Lines With Different Transformation Degree

Role of Dietary Fat in Ultraviolet Light–Induced Carcinogenic Expression

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