Breast Cancer Diet

A modified Mediterranean diet with particular attention paid to soy and greens. Avoid excess supplements?

Nutr Cancer. 2013;65(6):820-6. doi: 10.1080/01635581.2013.804939.

Are diet quality scores after breast cancer diagnosis associated with improved breast cancer survival?

Izano MA, Fung TT, Chiuve SS, Hu FB, Holmes MD.

Source

The Channing Division of Network Medicine, Department of Medicine , Brigham and Women's Hospital and Harvard Medical School , Boston , Massachusetts , USA.

Abstract

Previous studies have found that diets rich in fruits and vegetables are associated with reduced breast cancer mortality. However, these eating patterns do not necessarily reflect overall diet quality. The association of breast cancer mortality with a priori defined dietary scores, which are based on recommended dietary guidelines and reflect diet quality, has not been evaluated. We hypothesized that diet quality indices based on recommended guidelines are associated with decreased risk of breast cancer and nonbreast cancer mortality in breast cancer survivors. We examined the association between the Dietary Approaches to Stop Hypertension (DASH) score, and the Alternative Healthy Eating Index (AHEI)-2010, and the risk of breast cancer mortality and total mortality among women from the Nurses' Health Study diagnosed with breast cancer. Adherence to DASH-style and AHEI-2010 diets were associated with reduced risk of nonbreast cancer mortality (comparing the fifth quintile with the first quintile, relative risk (RR) = 0.72, 95% confidence interval (CI): 0.53-0.99, P trend = 0.03 for DASH, and RR = 0.57, 95% CI: 0.42-0.77, P trend <0.0001 for AHEI-2010). Diet scores were not significantly associated with breast cancer mortality. Our findings suggest that adherence to a higher quality diet after breast cancer diagnosis does not considerably change the risk of breast cancer death and recurrence. However, healthy dietary choices after breast cancer were associated with reduced risk of nonbreast cancer mortality in women with breast cancer.

PMID: 23909725

Nutr Cancer. 2011;63(3):381-8. doi: 10.1080/01635581.2011.535963.

Diet quality indices and postmenopausal breast cancer survival.

Kim EH, Willett WC, Fung T, Rosner B, Holmes MD.

Source

Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts 02115, USA. ehjkim@post.harvard.edu

Abstract

Research on diet in breast cancer survival has been focused on single nutrients or foods, particularly dietary fat, fruits, vegetables, fiber, and alcohol. We hypothesized that diet quality indices decrease the risk of total and non-breast-cancer-related deaths in women diagnosed with breast cancer. We evaluated 4 dietary quality scores: Alternate Healthy Eating Index (AHEI), Diet Quality Index-Revised (DQIR), Recommended Food Score (RFS), and the alternate Mediterranean Diet Score (aMED), among 2,729 women from the Nurses' Health Study with invasive Stage 1-3 breast cancer diagnosed between 1978 and 1998 with follow-up through 2004. In multivariate adjusted analyses, no association was found between diet quality indices and either total or non-breast-cancer-related deaths. However, a higher aMED score was associated with a lower risk of non-breast-cancer death in women with low physical activity; the RR comparing the highest to lowest tertile was 0.39 (95% CI, 0.20-0.75, P trend = 0.0004). Our results suggest that a higher-quality diet after breast cancer diagnosis does not considerably change the risk of death from breast cancer. However, healthy dietary choices may be important because women are at risk of death from non-breast-cancer-related causes affected by diet.

PMID: 21462090

Breast Cancer Res Treat. 2013 Sep 17. [Epub ahead of print]

Vegetable protein and vegetable fat intakes in pre-adolescent and adolescent girls, and risk for benign breast disease in young women.

Berkey CS, Willett WC, Tamimi RM, Rosner B, Frazier AL, Colditz GA.

Source

Channing Division of Network Medicine, Department of Medicine, Brigham & Women's Hospital and Harvard Medical School, Boston, MA, USA, catherine.berkey@channing.harvard.edu.

Abstract

Previous investigations, of adolescent diet recalled in adulthood, found lower risk for benign breast disease (BBD) with higher intakes of vegetable fat and nuts during high school. We investigate whether vegetable protein and fat, derived from diets reported during pre-adolescence and adolescence, are associated with subsequent risk for BBD in young women. The Growing Up Today Study includes 9,039 females, 9-15 years in 1996, who completed questionnaires annually through 2001, and then in 2003, 2005, 2007, and 2010. Food frequency questionnaires (1996-2001) obtained intake data on a variety of foods. Beginning in 2005, women (18-30 years) reported whether they had ever been diagnosed with BBD that was confirmed by breast biopsy (n = 112 cases). Logistic regression estimated associations between intakes of vegetable protein and fat and biopsy-confirmed BBD. Those individual foods that were the largest contributors of protein and fat in this cohort were also investigated. In analyses of intakes from 1996 through 1998, when our cohort was youngest, vegetable fat (OR = 0.72/(10 gm/day), 95 % CI 0.53-0.98; p = 0.04) was inversely associated with BBD risk. The greatest sources of vegetable fat and protein in these girls were peanut butter, peanuts, nuts, beans (beans, lentils, and soybeans), and corn. A daily serving of any one of these was associated with lower risk (OR = 0.32/(serv/day), 95 % CI 0.13-0.79; p = 0.01). Peanut butter (and nuts) at age 11 years was inversely associated with risk (p = 0.01). In analyses of intakes at age 14 years, vegetable protein was associated with lower BBD risk (OR = 0.64/(10 gm/day), 95 % CI 0.43-0.95; p = 0.03). A daily serving at 14 years of any one of the foods was associated with lower risk (OR = 0.34, 95 % CI 0.16-0.75; p = 0.01), as was peanut butter (and nuts) (p = 0.02). Girls with a family history of breast cancer had significantly lower risk if they consumed these foods or vegetable fat. In conclusion, consumption of vegetable protein, fat, peanut butter, or nuts by older girls may help reduce their risk of BBD as young women.

PMID: 24043428

Mol Carcinog. 2013 Sep 4. doi: 10.1002/mc.22074. [Epub ahead of print]

Dietary fat without body weight gain increases in vivo MCF-7 human breast cancer cell growth and decreases natural killer cell cytotoxicity.

Lamas B, Nachat-Kappes R, Goncalves-Mendes N, Mishellany F, Rossary A, Vasson MP, Farges MC.

Source

Clermont Université, Université d'Auvergne, Unité de Nutrition Humaine, Equipe ECREIN, CLARA, CRNH Auvergne, INRA, UMR 1019, Clermont-Ferrand, France.

Abstract

High-calorie (HC) diet contributes to the increased incidence of obesity, which is a risk factor for breast cancer in postmenopausal women, and in particular for estrogen receptor (ER) positive tumors. This study investigated whether an HC diet increases human ER-positive breast cancer progression and modulates natural killer (NK) cell functions. Four-week-old female BALB/c athymic nude mice were fed a HC diet (5320 kcal/kg) or standard calorie diet (SC, 2820 kcal/kg) for 6 mo. After 5 mo, the mice were randomly implanted with MCF-7 breast cancer cells (SCT and HCT) or received an isovolumic injection (SC and HC) in both inguinal fat pads. Tumor growth was greater in the HCT group than in the SC group without change in body weight. The HC diet decreased the tumor expression of genes involved in the citrate cycle and in adiponectin and lipid metabolism but increased that of genes controlling glycolysis and angiogenesis. The tumor expression level of Ki67 was increased while that of the cleaved caspase 3 and the ER-β and progesterone receptors was reduced. Tumor development in response to the HC diet was associated with smaller numbers and lower cytotoxicity of splenic NK cells. These results indicate that an HC diet without body weight gain increases ER-positive breast cancer cell proliferation and reduces tumor apoptosis. The underlying mechanisms might involve a downexpression of tumor hormonal receptor and reduced NK cell functions, and might also result in the regulation of genes involved in several cellular functions. © 2013 Wiley Periodicals, Inc.

KEYWORDS:

NK cells, high-calorie diet, human breast carcinoma xenograft

PMID: 24038423

BMC Cancer. 2013 Sep 13;13(1):418. [Epub ahead of print]

Characterization of synergistic anti-cancer effects of docosahexaenoic acid and curcumin on DMBA-induced mammary tumorigenesis in mice.

Siddiqui RA, Harvey KA, Walker C, Altenburg J, Xu Z, Terry C, Camarillo I, Jones-Hall Y, Mariash C.

Abstract

BACKGROUND:

The major obstacles to the successful use of individual nutritional compounds as preventive or therapeutic agents are their efficacy and bioavailability. One approach to overcoming this problem is to use combinations of nutrients to induce synergistic effects. The objective of this research was to investigate the synergistic effects of two dietary components: docosahexaenoic acid (DHA), an omega-3 fatty acid present in cold-water fish, and curcumin (CCM), an herbal nutrient present in turmeric, in an in vivo model of DMBA-induced mammary tumorigenesis in mice.

METHODS:

We used the carcinogen DMBA to induce breast tumors in SENCAR mice on control, CCM, DHA, or DHA + CCM diets. Appearance and tumor progression were monitored daily. The tumors were harvested 15 days following their first appearance for morphological and immunohistological analysis. Western analysis was performed to determine expression of maspin and survivin in the tumor tissues. Characterization of tumor growth was analyzed using appropriate statistical methods. Otherwise all other results are reported as mean +/- SD and analyzed with one-way ANOVA and Tukey's post hoc procedure.

RESULTS:

Analysis of gene microarray data indicates that combined treatment with DHA + CCM altered the profile of "PAM50" genes in the SK-BR-3 cell line from an ER-/Her-2+ to that resembling a "normal-like" phenotype. The in vivo studies demonstrated that DHA + CCM treatment reduced the incidence of breast tumors, delayed tumor initiation, and reduced progression of tumor growth. Dietary treatment had no effect on breast size development, but tumors from mice on a control diet (untreated) were less differentiated than tumors from mice fed CCM or DHA + CCM diets. The synergistic effects also led to increased expression of the pro-apoptotic protein, maspin, but reduced expression of the anti-apoptotic protein, survivin.

CONCLUSIONS:

The SK-BR-3 cells and DMBA-induced tumors, both with an ER- and Her-2+ phenotype, were affected by the synergistic interaction of DHA and CCM. This suggests that the specific breast cancer phenotype is an important factor for predicting efficacy of these nutraceuticals. The combination of DHA and CCM is potentially a dietary supplemental treatment for some breast cancers, likely dependent upon the molecular phenotype of the cancer.

PMID: 24034496

Br J Cancer. 2013 Sep 10. doi: 10.1038/bjc.2013.544. [Epub ahead of print]

The association between different night shiftwork factors and breast cancer: a case-control study.

Fritschi L, Erren TC, Glass DC, Girschik J, Thomson AK, Saunders C, Boyle T, El-Zaemey S, Rogers P, Peters S, Slevin T, D'Orsogna A, de Vocht F, Vermeulen R, Heyworth JS.

Source

Western Australian Institute for Medical Research, The University of Western Australia, Nedlands, Western Australia, Australia.

Abstract

Background:Research on the possible association between shiftwork and breast cancer is complicated because there are many different shiftwork factors, which might be involved including: light at night, phase shift, sleep disruption and changes in lifestyle factors while on shiftwork (diet, physical activity, alcohol intake and low sun exposure).Methods:We conducted a population-based case-control study in Western Australia from 2009 to 2011 with 1205 incident breast cancer cases and 1789 frequency age-matched controls. A self-administered questionnaire was used to collect demographic, reproductive, and lifestyle factors and lifetime occupational history and a telephone interview was used to obtain further details about the shiftwork factors listed above.Results:A small increase in risk was suggested for those ever doing the graveyard shift (work between midnight and 0500 hours) and breast cancer (odds ratio (OR)=1.16, 95% confidence interval (CI)=0.97-1.39). For phase shift, we found a 22% increase in breast cancer risk (OR=1.22, 95% CI=1.01-1.47) with a statistically significant dose-response relationship (P=0.04). For the other shiftwork factors, risks were marginally elevated and not statistically significant.Conclusion:We found some evidence that some of the factors involved in shiftwork may be associated with breast cancer but the ORs were low and there were inconsistencies in duration and dose-response relationships.British Journal of Cancer advance online publication, 10 September 2013; doi:10.1038/bjc.2013.544 www.bjcancer.com.

PMID: 24022188

Cancer Epidemiol Biomarkers Prev. 2013 Sep 9. [Epub ahead of print]

Equol producing status, isoflavone intake, and breast density in a sample of US Chinese women.

Tseng M, Byrne C, Kurzer MS, Fang CY.

Source

California Polytechnic State University.

Abstract

Background: Differences in ability to metabolize daidzein to equol might help explain inconsistent findings regarding isoflavones and breast cancer. We examined equol producing status in relation to breast density, a marker of breast cancer risk, and evaluated whether an association of isoflavone intake with breast density differs by equol producing status in a sample of Chinese immigrant women. Methods: Participants were 224 women, age 36-58 years, enrolled in a study on diet and breast density. All women completed dietary recall interviews, underwent a soy challenge to assess equol producing status, and received a mammogram assessed for breast density using a computer-assisted method. Results: In our sample, 30% were classified as equol producers. In adjusted linear regression models, equol producers had significantly lower mean dense tissue area (32.8 vs. 37.7 cm2, p=0.03) and lower mean percent breast density (32% vs. 35%, p=0.03) than non-producers. Significant, inverse associations of isoflavone intake with dense area and percent density were apparent, but only in equol producers (interaction p=0.05 for both). Conclusions: These results support the possibility that equol producing status affects breast density, and that effects of isoflavones on breast density depend on ability to metabolize daidzein to equol. Impact: While these findings warrant confirmation in a larger sample, they offer a possible explanation for the inconsistent findings regarding soy intake and breast density and possibly also breast cancer risk. The findings further suggest the importance of identifying factors that influence equol producing status, and exploring appropriate targeting of interventions.

PMID: 24019393

S-equol is produced by intestinal bacteria in some, but not in all, humans after soy consumption. The ability of S-equol to play a role in the treatment of estrogen or androgen-mediated diseases or disorders was first proposed in 1984

Cancer Sci. 2013 Aug 28. doi: 10.1111/cas.12268. [Epub ahead of print]

Lactobacillus casei Shirota enhances the preventive efficacy of soymilk in chemically induced breast cancer.

Kaga C, Takagi A, Kano M, Kado S, Kato I, Sakai M, Miyazaki K, Nanno M, Ishikawa F, Ohashi Y, Toi M.

Source

Yakult Central Institute for Microbiological Research, Tokyo, Japan.

Abstract

Soy foods are known to be effective for breast cancer prevention. The habitual consumption of soy isoflavones in combination with probiotic Lactobacillus casei Shirota (LcS) was shown to decrease the risk of breast cancer occurrence in our previous population-based case-controlled study among Japanese women. The present study aimed to elucidate the cooperative prevention mechanism of soymilk and LcS using an animal carcinogenic model. Female Sprague-Dawley rats received a high-fat, AIN-76A diet containing soymilk, LcS, both soymilk and LcS, or none and were orally exposed to 2-amino1-methyl-6-penylimidazo[4,5-b]pyridine at a dose of 85 mg/kg body weight 8 times for 2 weeks. The development of palpable mammary tumors was monitored for 17 weeks. Tumor tissues were immunohistochemically examined for estrogen receptor (ER)-α, Ki-67 and CD34. Compared with the control group, the incidence and the multiplicity of the mammary tumors were reduced by soymilk alone and soymilk in combination with LcS, while the tumor volume was decreased by LcS alone and LcS in combination with soymilk. An immunohistochemical analysis revealed that soymilk in combination with LcS more effectively reduced the numbers of ER-α-positive and Ki-67-positive cells in tumor than soymilk alone and that each soymilk and LcS inhibited the tumor angiogenesis. These results demonstrated that soymilk prevents the development of mammary tumors and that LcS suppresses tumor growth, potentially enhancing the preventive efficacy of soymilk. The habitual consumption of LcS in combination with soymilk might be a beneficial dietary style for breast cancer prevention. This article is protected by copyright. All rights reserved.

PMID: 23992486

Oncol Rep. 2000 Sep-Oct;7(5):977-82.

The effect of an oral administration of Lactobacillus casei strain shirota on azoxymethane-induced colonic aberrant crypt foci and colon cancer in the rat.

Yamazaki K, Tsunoda A, Sibusawa M, Tsunoda Y, Kusano M, Fukuchi K, Yamanaka M, Kushima M, Nomoto K, Morotomi M.

Source

Second Department of Surgery, School of Medicine, Showa University, Shinagawa-ku, Tokyo 142-8666, Japan.

Abstract

The preventive effect of oral administration of viable Lactobacillus casei strain Shirota (LcS) on azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF) and colon cancers in the rat was investigated. The study consisted of two experiments; in a short-term experiment (Exp-I), the inhibitory effect of 8- and 12-week treatments with LcS. Forty rats each received weekly a subcutaneous injection of AOM at a dose of 15 mg/kg of body weight for 5 weeks. Eight and twelve weeks after the start of the carcinogen treatment, each subgroup of rats were sacrificed, and the colon and the mesenteric lymph nodes (MLN) were removed. The number of ACFs and the surface marker of lymphocytes derived from the MLN were investigated. The large ACF (those comprising four or more aberrant crypts per focus) had significantly decreased in the rats which had consumed the LcS diet. And oral administration of viable LcS significantly recovered CD8 positive lymphocytes to the levels in the control group. In a long-term experiment (Exp-II), 30 rats each received weekly a subcutaneous injection of AOM at a dose of 7. 4 mg/kg of body weight for 10 weeks. Twenty-five weeks after the start of the carcinogen treatment, each subgroup of rats were sacrificed, and the colon were removed. The number and incidence of colon cancers were investigated. The number of rats with colon cancers and the number of colon cancers per rat, were significantly decreased in the rats which had consumed the LcS diet. LcS inhibited chemically-induced colon carcinogenesis in the rat. CD8 positive T lymphocytes may play a key role in the preventive effect against colon carcinogenesis.

PMID: 10948325

Clin Nutr. 2013 Aug 15. pii: S0261-5614(13)00206-9. doi: 10.1016/j.clnu.2013.08.001. [Epub ahead of print]

A comprehensive metabolic evaluation reveals impaired glucose metabolism and dyslipidemia in breast cancer patients early in the disease trajectory.

Bell KE, Di Sebastiano KM, Vance V, Hanning R, Mitchell A, Quadrilatero J, Russell C, Dubin JA, Bahl M, Califaretti N, Campbell C, Mourtzakis M.

Source

Department of Kinesiology, University of Waterloo, Burt Matthew Hall Rm. 1117, 200 University Avenue W., Waterloo, ON N2J 3G1, Canada.

Abstract

BACKGROUND & AIMS:

Weight gain in breast cancer patients during treatment is prevalent; the metabolic implications of this weight gain are poorly understood. We aimed to characterize glucose metabolism in breast cancer patients near the initiation of chemotherapy.

METHODS:

Stage I-II breast cancer patients (n = 8) were evaluated near the initiation of chemotherapy and compared with a group of age- and body mass index-matched, as well as a group of young healthy, non-malignant females. Fasting blood samples (analyzed for lipids and cytokines) were taken and an oral glucose tolerance test was performed. Body composition, waist circumference, diet, cardiovascular fitness and muscle strength were evaluated.

RESULTS:

Breast cancer patients were abdominally obese (mean ± SD: 94.6 ± 14.0 cm), overweight (28.8 ± 6.0 kg/m2) and dyslipidemic (triacylglycerides: 1.84 ± 1.17 mM; high-density lipoprotein cholesterol: 1.08 ± 0.23 mM). Compared to non-malignant matched females, fasting glucose and insulin concentrations were similar but fasting c-peptide was greater in patients (2.6 ± 1.2 ng/mL vs. 1.9 ± 0.8 ng/mL, p = 0.005). Glucose was elevated to a greater extent in patients during the oral glucose tolerance test compared with all non-malignant females. During the glucose tolerance test, c-peptide, but not insulin, remained elevated in patients compared with all non-malignant females. No differences in body composition, serum cytokines, nutrition or exercise capacity between patients and matched, non-malignant females emerged.

CONCLUSIONS:

Breast cancer patients present with unhealthy metabolic features early in the disease trajectory. Future investigations need to examine the underlying mechanisms and the potential longitudinal changes following chemotherapy.

KEYWORDS:

AUC, BMI, Body composition, CRP, Cytokines, DBP, EDTA, Exercise, HDL-c, IDF, IL, Insulin, International Diabetes Federation, LDL-c, NCEP-ATPIII, NEFA, National Cholesterol Education Program – Third Adult Treatment Panel, Nutrition, OGTT, PAQ, SBP, TAG, TNF-α, VO(2peak), area under the curve, body mass index, c-Peptide, c-reactive protein, diastolic blood pressure, ethylenediaminetetraacetic acid, high-density lipoprotein cholesterol, interleukin, low-density lipoprotein cholesterol, non-esterified fatty acid, oral glucose tolerance test, peak oxygen uptake, physical activity questionnaire, systolic blood pressure, triacylglycerol, tumor necrosis factor-α

PMID: 24011971

Int J Cancer. 2013 Aug 30. doi: 10.1002/ijc.28466. [Epub ahead of print]

Associations of dietary folate, vitamin B6, B12 and methionine intake with risk of breast cancer among African American (AA) and European American (EA) women.

Gong Z, Ambrosone CB, McCann SE, Zirpoli G, Chandran U, Hong CC, Bovbjerg DH, Jandorf L, Ciupak G, Pawlish K, Lu Q, Hwang H, Khoury T, Wiam B, Bandera EV.

Source

Department of Cancer Prevention & Control, Roswell Park Cancer Institute, Buffalo, NY.

Abstract

African American (AA) women are more likely than European American (EA) women to be diagnosed with breast cancer at younger ages and to develop poor prognosis tumors. However, these racial differences are largely unexplained. Folate and other methyl-group nutrients may be related to breast carcinogenesis, but few studies have examined these associations in AA populations. We examined the associations of dietary intake of these nutrients with breast cancer risk overall, by menopausal and estrogen receptor (ER) status among 1,582 AA (749 cases) and 1,434 EA (744 cases) women using data from a case-control study, the Women's Circle of Health Study. Unconditional multivariable logistic regression models were used to compute odds ratios (ORs) and 95% confidence intervals (CIs) for the association of each nutrient and breast cancer risk. In AA women, inverse associations were observed for natural food folate intake among premenopausal women (4th vs. 1st quartile: OR=0.57, 95% CI, 0.33-1.00; P for trend=0.06) and for ER positive tumors (4th vs. 1st quartile: OR=0.58, 95% CI, 0.36-0.93; P for trend=0.03), whereas in EA women, a positive association was observed for intake of synthetic folate (4th vs. 1st quartile: OR=1.53, 95% CI, 1.06-2.21; P for trend=0.03). Our findings suggest that natural food folate intake is inversely associated with breast cancer risk and that this association may vary by race, menopausal or ER status. The finding of an increased risk observed among EA women with the highest intake of synthetic folate from fortified foods warrants further investigation. © 2013 Wiley Periodicals, Inc.

KEYWORDS:

African American, European American, breast cancer, diet, folate, one-carbon nutrients

PMID: 23996837

Expert Opin Ther Targets. 2013 Sep 14. [Epub ahead of print]

Molecular mechanisms of the pro-apoptotic actions of melatonin in cancer: a review.

Bizzarri M, Proietti S, Cucina A, Reiter RJ.

Source

University La Sapienza, Department of Experimental Medicine, Systems Biology Group , Rome , Italy mariano.bizzarri@uniroma1.it.

Abstract

Introduction: Compelling evidence has highlighted the complex pleiotropic functions elicited by the melatonin in cancer cells. Melatonin behaves as a 'smart killer', i.e., modulating anti-apoptotic processes in normal cells, and triggering pro-apoptotic signals in cancer cells. Areas covered: Melatonin induces programmed cell death in a wide range of different tumors (breast, gastro-intestinal, hematological, prostate, osteosarcoma, melanoma, kidney, etc…). Mechanisms of action and molecular pathways involved in pro-apoptotic processes under melatonin treatment are discussed. Expert opinion: Melatonin involvement in apoptotic processes is a new and relevant field of investigation. Even in tumor models unresponsive to melatonin alone, this hormone can significantly amplify the cytostatic and the cytotoxic effects triggered by other compounds or conventional drugs. We are far from having a satisfactory understanding about how and when melatonin exerts its beneficial effects. Melatonin in the nanomolar range activates the intrinsic and/or the extrinsic apoptotic pathway in cancer cells, namely through an increase in the p53/MDM2p ratio and downregulation of Sirt1. This finding is of great relevance since there is intense research ongoing to identify nontoxic feasible inhibitors of MDM2 and Sirt1. Melatonin should be evaluated for the management of those cancers where both of these are overexpressed and functionally strategic.

PMID: 24032643

J Pineal Res. 2013 Apr;54(3):334-45. doi: 10.1111/jpi.12032. Epub 2013 Jan 17.

Expression of melatonin receptor MT1 in cells of human invasive ductal breast carcinoma.

Jablonska K, Pula B, Zemla A, Owczarek T, Wojnar A, Rys J, Ambicka A, Podhorska-Okolow M, Ugorski M, Dziegiel P.

Source

Department of Histology and Embryology, Wroclaw Medical University, Wroclaw, Poland.

Abstract

In humans, two main types of membrane melatonin receptors have been identified, MT1 and MT2. Expression of MT1 in neoplastic cells seems to increase the efficacy of melatonin's oncostatic activity. The purpose of this study was to determine the distribution and the intensity of MT1 expression in breast cancer cells and to correlate it with clinicopathological factors. Immunohistochemical studies (IHC) were conducted on 190 cases of invasive ductal breast carcinomas (IDC) and molecular studies were performed on 29 cases of frozen tumor fragments and selected breast cancer cell lines. Most of the studied tumors manifested a membranous/cytoplasmic IHC expression of MT1. In IDC, the MT1 expression was higher than in fibrocystic breast disease. MT1 expression was higher in estrogen receptor positive (ER+) and HER2 positive (HER2+) tumors. Triple negative tumors (TN) manifested the lowest MT1 expression level. The lowest MT1 protein expression level was noted in the TN breast cancer cell line MDA-MB-231 compared with ER+ cell lines MCF-7 and SK-BR-3. MT1 mRNA expression was negatively correlated with the malignancy grade of the studied IDC cases. Moreover, higher MT1 expression was associated with patients' longer overall survival (OS) in the group of ER+ breast cancers and treated with tamoxifen. Multivariate analysis indicated that MT1 was an independent prognostic factor in the ER+ tumors for OS and event-free survival in the ER+ tumors. The results of this study may point to a potential prognostic and therapeutic significance of MT1 in IDC.

PMID: 23330677