Effects of a high olive oil diet on the clinical behavior and histopathological features of rat DMBA-induced mammary tumors compared with a high corn oil diet

Solanas, Montserrat; Hurtado, Antoni; Costa, Irmgard; Moral, Raquel; Menéndez, Javier A.; Colomer, Ramon; Escrich, Eduard

doi:10.3892/ijo.21.4.745

Cited by 49 publications

(51 citation statements)

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“…Tumors appearing in this rat mammary model are histologically and biochemically similar to human tumors [Escrich, 1987a;Escrich, 1987b;Russo et al, 1990]. Additional features that make this model the most widely used as an experimental mammary tumor system are tumor induction ease and reliability, organ site specificity, tumors of ductal origin, tumors of predominantly carcinomatous histopathological characteristics, tumors of varying growth factor and/or hormone responsiveness, and the potential to examine the tumor initiation and promotion processes [Welsch, 1985;Russo and Russo, 1996;Izzotti et al, 1999;Cabello et al, 2001;Kubatka et al, 2002;Solanas et al, 2002;Moral et al, 2003]. Previous work indicates that the induction of mammary carcinogenesis in the rat by DMBA depends on the age of the animals and the extent of differentiation of the mammary gland, at the time the carcinogen is administered [Russo and Russo, 1978;Welsch, 1985].…”

Section: Discussionmentioning

confidence: 99%

Induction of cell proliferation, micronuclei and hyperdiploidy/polyploidy in the mammary cells of DDT- and DMBA-treated pubertal rats

Uppala

Roy

Tousson

et al. 2005

Environ. Mol. Mutagen.

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The environmental estrogen, dichlorodiphenyltrichloroethane (DDT), and its metabolites have been implicated in the development of breast cancer through mechanisms that remain to be elucidated. It has been hypothesized that exposure to DDT and its metabolites, during critical periods of development, can contribute to an elevated risk for breast cancer in adults. In the present study, we have investigated the effect of o,p'-DDT on mammary gland cell proliferation and chromosomal alterations, in a rat mammary cancer model (commonly used to study human cancer), to gain insights into its potential role in the development of breast cancer. Twenty-one-day-old female Sprague-Dawley (SD) rats were administered o,p'-DDT, 7,12-dimethylbenz[a]anthracene (DMBA), genistein, DDT+DMBA, or DDT+DMBA+genistein, over a 14-day period. To determine changes in chromosome number and structure, we used the micronucleus assay as well as multicolor fluorescence in situ hybridization (FISH) region-specific DNA probes for rat chromosomes 4 and 19. Cell proliferation was evaluated using 5-bromo-2'-deoxyuridine (BrdU). Significant increases in BrdU-incorporated cells were seen in the rats treated with DDT+DMBA. Although micronucleus frequencies were somewhat elevated in several of the treatment groups, significant increases were not seen in any of them. Significant increases in numerical chromosomal aberrations were detected in all of the DDT- and DMBA-treated groups. Genistein significantly reduced BrdU incorporation and polyploidy in the DDT+DMBA-treated rats. These initial studies indicate that DDT and DMBA can induce cellular and chromosomal alterations in the rat mammary gland, which is consistent with the hypothesis that these agents can induce early events in mammary carcinogenesis.

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Section: Discussionmentioning

confidence: 99%

Induction of cell proliferation, micronuclei and hyperdiploidy/polyploidy in the mammary cells of DDT- and DMBA-treated pubertal rats

Uppala

Roy

Tousson

et al. 2005

Environ. Mol. Mutagen.

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“…In vitro studies reported that exposure of breast cancer cells to oleic acid resulted in the down-regulation of Her-2/neu, an oncogene overexpressed in w20% of breast carcinomas (Menendez et al 2005a). In a rat model of dimethylbenz(a)anthracene-induced mammary carcinogenesis, a diet rich in olive oil resulted in a much slower progression of the Endocrine-Related Cancer (2010) 17 539-551 www.endocrinology-journals.org tumours (Solanas et al 2002, Costa et al 2004. Epidemiological data have also suggested an effect in women.…”

Section: Oleate Differentially Affects the Growth Of Malignant Cells mentioning

confidence: 99%

Hyperglycaemia confers resistance to chemotherapy on breast cancer cells: the role of fatty acid synthase

Zeng¹,

Biernacka²,

Holly³

et al. 2010

Endocrine-Related Cancer

102

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The prognosis for women with breast cancer is adversely affected by the comorbidities of obesity and diabetes mellitus (DM), which are conditions associated with elevated levels of circulating fatty acids, hyperglycaemia and hyperinsulinaemia. We investigated the effects of exposure of nonmalignant and malignant human breast epithelial cells to elevated levels of fatty acids and glucose on their growth, survival and response to chemotherapeutic agents. We found that palmitate induced cell death in the non-malignant cells but not in the malignant cells, which was abrogated through the inhibition of ceramide production and by oleate but not by IGF1. Fatty acid synthase (FAS) is responsible for the de novo synthesis of fatty acids from sugars, and is over-expressed in many epithelial cancers. Abundance of FAS was higher in malignant cells than in non-malignant cells, and was up-regulated by IGF1 in both cell types. IGF-induced growth of non-malignant cells was unaffected by suppression of FAS expression, whereas that of malignant cells was blocked as was their resistance to palmitate-induced cell death. Palmitate did not affect cell proliferation, whereas oleate promoted the growth of non-malignant cells but had the opposite effect, that is, inhibition of IGF1-induced growth of malignant cells. However, when the phosphatidylinositol 3-kinase pathway was inhibited, oleate enhanced IGF1-induced growth in both cell types. Hyperglycaemia conferred resistance on malignant cells, but not on non-malignant cells, to chemotherapy-induced cell death. This resistance was overcome by inhibiting FAS or ceramide production. Understanding the mechanisms involved in the associations between obesity, DM and breast cancer may lead to more effective treatment regimens and new therapeutic targets.

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“…In all the experimental studies developed in our laboratory, the high-EVOO diet, in comparison with the HCO diet, consistently increased tumour latency (retarding the appearance of tumours) and decreased tumour incidence, multiplicity and volume (7,22,(30)(31)(32)(33) . Moreover, in some of the experimental series, we have observed that the olive oil diet reduced tumour content and volume, even in comparison with a control low-fat diet, which suggested a protective effect of the olive oil on mammary carcinogenesis (22,33) . The study of tumour regression, as a proposed protective effect of this higholive oil diet, showed a slow progression of tumours in the animals fed that diet, rather than a real regression (22) .…”

Section: Effects Of Extra Virgin Olive Oil On Experimental Breast Canmentioning

confidence: 79%

“…In sixteen experimental series developed in our laboratory, results have always been conclusive: diets with a high content of n-6 PUFA (corn oil) exert a clear stimulating effect of the experimental mammary carcinogenesis in all the clinical parameters studied (22,(27)(28)(29)(30)(31) (Fig. 1).…”

Section: Effects Of Extra Virgin Olive Oil On Experimental Breast Canmentioning

confidence: 93%

Olive oil, an essential component of the Mediterranean diet, and breast cancer

Escrich

Moral

Solanas

2011

Public Health Nutr.

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Objective: The Mediterranean diet has been related to a lower risk of some chronic diseases, including cancer. We aim to gain insight into the effects of the main source of fat of this diet on breast cancer, the most common type of malignancy in women. Design: Data from sixteen experimental series analysing the effects of dietary lipids on mammary carcinogenesis in an animal model, in the context of the international literature on the Mediterranean diet, olive oil and breast cancer risk. Setting: Experimental and human data on the effects of olive oil and Mediterranean diet on breast cancer. Subjects: An animal model of induced breast cancer and other human and experimental studies in the literature.Results: Diets rich in extra virgin olive oil (EVOO) exert a negative modulatory effect on experimental breast cancer to a weak promoting effect, much lower than that obtained with a high-corn oil diet. EVOO confers to the mammary adenocarcinomas a clinical behaviour and morphological features compatible with low tumour aggressiveness. This differential effect, in relation to other dietary lipids, may be related to a lower effect on body weight and sexual maturation. In addition, EVOO induced different molecular changes in tumours, such as in the composition of cell membranes, activity of signalling proteins and gene expression. All these modifications could induce lower proliferation, higher apoptosis and lower DNA damage. These results, together with the favourable effect of olive oil reported in the literature when it is consumed in moderate quantities, suggest a beneficial influence of EVOO on breast cancer risk. Conclusions: Consumption of EVOO in moderate quantities and throughout the lifetime appears to be a healthy choice and may favourably influence breast cancer risk.

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Effects of a high olive oil diet on the clinical behavior and histopathological features of rat DMBA-induced mammary tumors compared with a high corn oil diet

Cited by 49 publications

References 0 publications

Induction of cell proliferation, micronuclei and hyperdiploidy/polyploidy in the mammary cells of DDT- and DMBA-treated pubertal rats

Induction of cell proliferation, micronuclei and hyperdiploidy/polyploidy in the mammary cells of DDT- and DMBA-treated pubertal rats

Hyperglycaemia confers resistance to chemotherapy on breast cancer cells: the role of fatty acid synthase

Olive oil, an essential component of the Mediterranean diet, and breast cancer

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