What Should ER+/PR- Breast Cancer Patients And Survivors Eat?

What should ER+/PR- breast cancer patients and survivors eat?

Last updated: July 6, 2010

Up to 15% of invasive breast cancers are classified as estrogen receptor positive and progesterone receptor negative, or ER+/PR-. In other words, the relevant genes cause the cancer cells to express estrogen receptors, but not progesterone receptors. Compounds that regulate ER or PR expression, oppose the production of estrogen in the body (i.e., oppose aromatase) or inhibit estrogen binding to estrogen receptors are among those used to treat this type of breast cancer. Tumors with a large number of estrogen receptors are associated with a better the prognosis than those with few. However, ER+/PR- breast cancer patients may be more likely than ER+/PR+ patients to benefit from epidermal growth factor receptor (EGFR) inhibitors and possibly from foods that inhibit the EGFR receptor. Please discuss this article with your oncologist.

Significant associations have been found between carbohydrate intake, glycemic index and glycemic load and higher risk of ER+/PR- breast cancer. This suggests that women with ER+/PR- breast cancer should avoid foods such as white bread, cakes and sugar, as well as refraining from eating meals with a high overall glycemic load. Pan-fried red meat has also been found to be associated with higher risk of ER+/PR- breast cancer.

Foods that increase the risk of ER+/PR- breast cancer

The following foods (as well as other foods not listed that have a high glycemic load) can increase the risk of ER+/PR- breast cancer:

Bread, white

Cookies, candy and cake

Cornflakes and similar breakfast cereals

Granola

Plantains, fried ripe

Foods that may reduce the risk of ER+/PR- breast cancer

The following foods have been associated with reduced risk of breast cancer in general. These foods also have components that have been shown to inhibit the EGFR receptor, thereby having the potential to prevent ER+/PR- breast cancer or its recurrence in particular:

While folate might promote breast cancer in some cases, dietary folate has been found to be inversely associated with the risk of ER+/PR- breast cancer. In addition to some of the brassica vegetables listed above, the following foods are good sources of folate while also having been found to be associated with reduced risk of breast cancer:

Additional comments

Several studies have found that in some cases when the original breast cancer is ER+, the subsequent metastatic breast cancer is ER-. Therefore, it is important for ER+/PR- breast cancer patients and survivors to eat a wide variety of the foods on our recommended food list and limit or avoid those on our avoid list, in addition to paying particular attention to the foods on the lists above.

Tags: ChineseCabbage, ER+, ER+/PR-, ER-, HRT, PR-, arugula, beef, blueberries, bokChoy, bread, broccoli, brusselsSprouts, cabbage, carrots, cauliflower, celery, cherries, chicken, collardGreens, cranberries, dryBeans, folate, glycemicIndexLoad, grapes, greenTea, hormoneReplacementTherapy, horseradish, hotPeppers, kale, lettuce, mustard, oats, onions, overweight, parsley, plantains, pomegranates, pork, potatoes, raspberries, redMeat, rice, saffron, seaweed, serotonin, soybeans, spinach, statins, sugar, tofu, turmeric, watercress, whatToEatByType

Selected studies

Vegetable intake is associated with reduced breast cancer recurrence in tamoxifen users: a secondary analysis from the Women's Healthy Eating and Living Study Breast Cancer Research and Treatment, July 2010 Thomson CA, Rock CL, Thompson PA, Caan BJ, Cussler E, Flatt SW, Pierce JP

The current prospective study was designed to investigate the association between breast cancer recurrence and vegetable intake, with a focus on the impact on those using tamoxifen. The protective effect of vegetables on the risk of breast cancer recurrence has not been established. Previous reports of anti-carcinogenic activity of phytochemicals in cruciferous vegetables in combination with tamoxifen led the authors to include specific evaluation of this class of vegetables in the study. The study included 3,080 breast cancer survivors enrolled in the Women's Healthy Eating and Living (WHEL) Study. Vegetable intake based on repeat 24-hour dietary recalls were examined as a secondary analysis in the cohort. The women were 23.5 months post-diagnosis, on average, at time of enrollment. The hazard of recurrence with vegetable intake was assessed in the overall study group and separately for women taking tamoxifen, while controlling for relevant clinical and demographic variables. Participants reported baseline average intakes of 3.1 +/- 0.05 servings per day of vegetables, and 0.5 +/- 0.02 servings per day of cruciferous vegetables. Vegetable intake was divided into thirds. Vegetable intake in the highest compared to the lowest thirds was found to be associated with a lower adjusted hazard ratio (HR) for breast cancer recurrence of 0.69 (95% confidence interval (CI) = 0.55-0.87). Among women taking tamoxifen, HR = 0.56 (95% CI = 0.41-0.77) for total vegetable intake and HR = 0.65 (95% CI = 0.47-0.89) for cruciferous vegetable intake. For women using tamoxifen who had above median cruciferous vegetable intake, as well as being within the highest third of total vegetable intake, HR = 0.48 (95% CI = 0.32-0.70). The authors conclude that baseline vegetable intake may be associated with a reduction in the risk of breast cancer recurrence or new events, particularly for those using tamoxifen. The associations deserve further study since it is possible that vegetable intake is simply a surrogate for other health-promoting behaviors.

Capsaicin causes cell-cycle arrest and apoptosis in ER-positive and -negative breast cancer cells by modulating the EGFR/HER-2 pathway Oncogene, October 2009

The present study was designed to evaluate the impact of capsaicin (trans-8-methyl-N-vanillyl-6-nonenamide) on breast cancer cells in vitro and in vivo. Capsaicin is found in chili peppers and has been reported to have inhibitory effects against various types of cancer cells in the laboratory. In the study, capsaicin was found to inhibit the growth of MCF-7, T47D, and BT-474 estrogen receptor positive (ER+) breast cancer cells, as well as SKBR-3 HER-2 overexpressing and MDA-MB231 (ER-/PR-) breast cancer cells. Growth inhibition was associated with G(0)/G(1) cell-cycle arrest, increased apoptosis, reduced expression of HER-2, and activated extracellular-regulated kinase and cyclin D1. Cell-cycle regulator p27(KIP1), caspase activity, and poly-ADP ribose polymerase cleavage all were observed to increase. Importantly, capsaicin also blocked breast cancer cell migration in vitro. In further experimentation, MDA-MB231 tumors were grown in immunodeficient mice. Capsaicin was found to reduce the size of the tumors in the mice by approximately half without evidence of toxicity. Activation of extracellular-regulated kinase was clearly attenuated in the tumors, as well as expression of HER-2 and cyclin D1. Caspase activity and poly-ADP ribose polymerase cleavage products were heightened in the tumors of mice treated with capsaicin. In addition, capsaicin treatment was found to powerfully inhibit the development of pre-neoplastic breast lesions by up to 80% without any apparent side effects. The authors conclude that capsaicin is a novel modulator of the EGFR/HER-2 pathway in both ER+ and ER- breast cancer cells and has a potential role in the treatment and prevention of breast cancer.

Fucoidan from Laminaria cichorioides inhibits AP-1 transactivation and cell transformation in mouse epidermal JB6 cells American Association for Cancer Research (AACR) Int'l Conference on Frontiers in Basic Cancer Research, October 2009

The present study was designed to evaluate the mechanism of action by which fucoidan, a sulfated polysaccaride extracted from brown seaweeds, exerts chemopreventive effects. Fucoidan has been shown to have anticoagulant and antithrombotic properties. In addition, unlike heparin (an anticoagulant), fucoidan is known to exhibit anticancer activities. In the study, fucoidan from Laminaria cichorioides, a type of brown algae, was shown to inhibit neoplastic cell transformation induced by epidermal growth factor or 12-O-tetradecanoylphorbol-13-acetate (a tumor promoter), but had less cytotoxic effect on JB6 mouse epidermal cells. The phosphorylation of extracellular signal-regulated kinases 1/2 and c-Jun N-terminal kinases normally induced by epidermal growth factor was inhibited by fucoidan. These results appeared to be due to the inhibition of phosphorylation of epidermal growth factor receptor. Fucoidan was shown to reduce c-fos or c-jun transcriptional activity in a dose-dependent manner, thereby attenuating the associated AP-1 transactivation activity. Further testing demonstrated that fucoidan directly interacted with epidermal growth factor, apparently preventing the binding of epidermal growth factor to its cell surface receptor. This could explain fucoidan's antitumor promoting effect. The authors comment that the study findings are the first to reveal a molecular basis for the anticarcinogenic action of fucoidan, which may partially account for the reported chemopreventive effects of brown seaweeds.

Conjugated linoleic acid intake and breast cancer risk in a prospective cohort of Swedish women American Journal of Clinical Nutrition, September 2009

The present prospective study was designed to investigate the association between intake of conjugated linoleic acids (CLAs) and the risk of breast cancer. Animal and in vitro studies suggest that CLAs, fatty acids found primarily in dairy products and in the meat of ruminants, have protective activities against mammary carcinogenesis. However, findings from population studies in relation to breast cancer risk are few and inconsistent. The study included 61,433 women in the Swedish Mammography Cohort who were cancer-free at enrollment during 1987 to 1990. Dietary CLA intake was determined by means of a food-frequency questionnaire at baseline. Cox proportional hazards models were used to calculate rate ratios (RRs) and 95% confidence intervals (CIs), adjusted for breast cancer risk factors. During a mean follow-up period of 17.4 years, 2,952 new cases of invasive breast cancer were diagnosed in the study group. No significant association was found between dietary CLA intake and risk of breast cancer, overall or by estrogen receptor (ER) and progesterone receptor (PR) status of the tumors. The multivariate relative risks (95% CI) for the highest fifth of CLA intake (155.7 mg/day) compared with the lowest quintile (<78.1 mg/day) were 1.04 (0.92 - 1.17) for overall breast cancer, 1.09 (0.90 - 1.31) for ER+/PR+ tumors, 1.09 (0.78 - 1.53) for ER+/PR- tumors, and 0.84 (0.57 - 1.24) for ER-/PR- tumors. The authors conclude that the results provide no evidence of a protective effect of CLA against breast cancer development in women.

Glycemic load, glycemic index and breast cancer risk in a prospective cohort of Swedish women International Journal of Cancer, July 2009

The present prospective study investigated the associations between carbohydrate intake, glycemic index and glycemic load and risk of breast cancer in the Swedish Mammography Cohort. High-glycemic load diets are thought to increase the risk of breast cancer but population studies have yielded inconsistent results. The study included 61,433 women who completed a food frequency questionnaire upon enrollment in the period 1987 to 1990. During a follow-up period averaging 17.4 years, 2,952 incident cases of invasive breast cancer were diagnosed. Glycemic load but not carbohydrate intake or glycemic index was found to be weakly positively associated with risk of breast cancer (p for trend = 0.05). When stratified by tumor estrogen receptor (ER) and progesterone receptor (PR) status, significant positive associations of carbohydrate intake, glycemic index and glycemic load with risk of ER+/PR- breast cancer were found: the multivariate relative risks comparing the highest and lowest quintiles of intake were 1.34 (95% confidence interval (CI) = 0.93-1.94; p for trend = 0.04) for carbohydrate intake, 1.44 (1.06-1.97; 0.01) for glycemic index and 1.81 (1.29-2.53; 0.0008) for glycemic load. No associations were seen for ER+/PR+ or ER-/PR- breast tumors. The authors conclude that a high carbohydrate intake and diets with high glycemic index and glycemic load may increase the risk of developing ER+/PR- breast cancer.

Alcohol and Risk of Breast Cancer by Histologic Type and Hormone Receptor Status in Postmenopausal Women American Journal of Epidemiology, June 2009 Jasmine Q. Lew, Neal D. Freedman, Michael F. Leitzmann, Louise A. Brinton, Robert N. Hoover, Albert R. Hollenbeck, Arthur Schatzkin, Yikyung Park

The present study was designed to examine the association between alcohol consumption and breast cancer in postmenopausal women by breast cancer type. The study group included 184,418 postmenopausal women 50 to 71 years old in the National Institutes of Health-AARP Diet and Health Study (1995–2003). A mailed questionnaire was used at baseline to assess alcohol use, diet, and potential risk factors for cancer. Relative risks and 95% confidence intervals were calculated by using Cox proportional hazards regression. State cancer registries were used to identify breast cancer cases and estrogen receptor and progesterone receptor status. During a mean seven year follow-up period, 5,461 breast cancer cases were identified. Alcohol consumption was found to be significantly positively associated with risk of breast cancer: Even a moderate amount of alcohol (greater than 10 g/day) was shown to significantly increase risk of breast cancer. In a comparison of greater than 35 g per day versus no alcohol intake, the multivariate relative risks were found to be 1.35 (95% confidence interval (CI): 1.17-1.56) for total breast cancer, 1.46 (95% CI: 1.22-1.75) for ductal breast cancer, and 1.52 (95% CI: 0.95-2.44) for lobular tumors. The multivariate relative risk for estrogen receptor-positive/progesterone receptor-positive (ER+/PR+) tumors was 1.46 (95% CI: 1.12-1.91) for greater than 35 g per day versus no alcohol intake. The estrogen receptor-positive/progesterone receptor-negative (ER+/PR-) multivariate relative risk was 1.13 (95% CI: 0.73-1.77) for greater than 20 g versus no alcohol intake. The estrogen receptor-negative/progesterone receptor-negative (ER-/PR-) multivariate relative risk was 1.21 (95% CI: 0.79-1.84) for greater than or equal to 20 g versus no alcohol intake. The authors conclude that moderate consumption of alcohol is associated with breast cancer, especially hormone receptor-positive tumors.

Long-term meat intake and risk of breast cancer by oestrogen and progesterone receptor status in a cohort of Swedish women European Journal of Cancer, May 2009

The present prospective population study was designed to examine the association between red meat intake and incidence of breast cancer defined by estrogen receptor (ER) and progesterone receptor (PR) status. The study included 61,433 women in the Swedish Mammography Cohort. Dietary intake was assessed during 1987–1990 (baseline) and again in 1997. Cox proportional hazards models were used to calculate relative risks. During a 17.4-year average follow-up period, 2,952 new invasive breast cancer cases were discovered. No significant associations were found between consumption of total red meat, fresh red meat or processed meat and risk of breast cancer. The multivariate relative risks (95% confidence interval) for the highest fifth of total red meat intake (98 g/day) compared with the lowest quintile (under 46 g/day) were 0.98, 95% CI: 0.86–1.12 for overall breast cancer, 1.10 (0.90–1.34) for ER+/PR+ tumors, 0.86 (0.60–1.23) for ER+/PR– and 1.12 (0.70–1.79) for ER–/PR–. However, intake of pan-fried meat was found to be positively associated with risk of ER+/PR– breast cancer; the multivariate relative risk for the highest compared with the lowest quartile of consumption was 1.45 (95% CI: 1.03–2.03; Ptrend = 0.03). The authors conclude that the results do not support an association between red meat consumption and overall breast cancer risk, but suggest that fried meat may increase the risk of ER+/PR– breast cancer.

Changes in estrogen receptor, progesterone receptor and her-2/neu status with time: discordance rates between primary and metastatic breast cancer Anticancer Research, May 2009

The current study was designed to determine receptor discordance rates between primary and metastatic breast cancer tissue using archival paired pathological samples. Data was obtained for 100 breast cancer cases for whom tissue from both primary and metastatic sites was available. Estrogen receptor (ER), progesterone receptor (PR) and Her-2/neu status were compared in the primary tumor versus the metastasis. The ER discordance rate was found to be 17.7%: 9.7% of tumors changed from ER+ to ER- and 8.0% changed from ER- to ER+. The PR discordance rate was found to be 37.3%: in all of these cases, the primary tumors was PR+ and the metastasis was PR-. No significant discordance was found for Her-2/neu expression. The authors conclude that significant discordance exists for hormone receptor status between primary and metastatic breast cancer.

Long-term dietary calcium intake and breast cancer risk in a prospective cohort of women American Journal of Clinical Nutrition, January 2009

The current prospective study was designed to examine the association between dietary calcium intake and breast cancer risk by estrogen receptor (ER) and progesterone receptor (PR) status of the tumor. Calcium is thought to potentially influence breast cancer risk since it has a role in regulating cell proliferation, differentiation, and apoptosis. The study included 61,433 women in the Swedish Mammography Cohort who were cancer-free at enrollment during 1987 to 1990. Dietary calcium intake was determined by means of a food-frequency questionnaire at baseline and again in 1997. Cox proportional hazards models were used to calculate rate ratios (RRs) and 95% confidence intervals (CIs), adjusted for breast cancer risk factors. During a mean follow-up period of 17.4 years, 2,952 new cases of invasive breast cancer were diagnosed in the study group. Dietary calcium intake was found not to be associated with breast cancer risk in the group overall; the multivariate RR for the highest compared with the lowest fifth of calcium intake was 0.97 (95% CI: 0.87 - 1.09; P for trend: 0.49). However, a statistically significant inverse trend for ER-negative/PR-negative (ER-/PR-) breast cancer (P for trend: 0.02) was observed; the multivariate RR for the comparison of the highest with the lowest quintiles of calcium intake was 0.66 (95% CI: 0.44 - 0.99). Calcium intake was not found to be associated with ER+/PR+ or ER+/PR- tumors. The authors conclude that their findings do not support an association between dietary calcium intake and overall breast cancer risk and that the inverse relation between calcium intake and ER-/PR- breast cancer requires confirmation in other studies.

Folate Intake and Risk of Breast Cancer by Estrogen and Progesterone Receptor Status in a Swedish Cohort Cancer Epidemiology, Biomarkers & Prevention, December 2008

The current study was designed to examine the association between dietary folate intake and the risk of breast cancer by estrogen receptor (ER) and progesterone receptor (PR) status of the tumor. Folate is a B vitamin involved in one-carbon metabolism that has been postulated to affect the risk of breast cancer. However, population studies of folate intake with regard to breast cancer risk are not conclusive. Study participants included 61,433 women in the Swedish Mammography Cohort who were cancer-free at enrollment during 1987 to 1990. Dietary folate intake was determined by means of a food-frequency questionnaire at baseline and again in 1997. Cox proportional hazards models were used to calculate rate ratios (RRs) and 95% confidence intervals (CIs), adjusted for breast cancer risk factors. During a mean follow-up period of 17.4 years, 2,952 new cases of invasive breast cancer were diagnosed in the study group. Dietary folate intake was not found to be associated with breast cancer risk in the group overall; the multivariate RR for the highest compared with the lowest fifth of calcium intake was 1.01 (95% CI: 0.90-1.13; P for trend: 0.84). There were also no observed associations between dietary folate intake and risk of ER+/PR+ or ER-/PR- tumors. However, folate intake was found to be inversely associated with the risk of ER+/PR- breast cancer (n = 417 cases; RR for highest versus lowest quintile = 0.79; 95% CI, 0.59-1.07; Ptrend = 0.01). The results did not vary by alcohol intake or menopausal status. The authors conclude that the study findings do not support an overall association between folate intake and risk of breast cancer but suggest that folate intake may be inversely associated with ER+/PR– tumors.

Risk factors for postmenopausal breast cancer defined by estrogen and progesterone receptor status: The multiethnic cohort American Association for Cancer Research (AACR) Meeting, April 2008

The current prospective study was designed to examine the associations of several known breast cancer risk factors by estrogen receptor (ER) and progesterone receptor (PR) status in the large prospective Multiethnic Cohort study. The study included 46,079 women with natural menopause or bilateral oophorectomy who provided risk data at baseline by means of a questionnaire. During a follow-up period averaging 8.3 years, 1,339 new cases of breast cancer were diagnosed for which information on ER/PR status was available. There were 902 women with ER+/PR+ breast cancer, 231 with ER-/PR-, 173 with ER+/PR-, and 33 with ER-/PR+. Hazard rate ratios (RRs) and 95% confidence intervals (CIs) for breast cancer incidence by ER/PR status associated with each risk factor were calculated using Cox log-linear proportional hazard models stratified by age at recruitment to the study, year of recruitment, race/ethnicity, and study area, and adjusted for potential confounders. Compared with women having a body mass index (BMI) of less than 25 kg/m2, those with BMIs of at least 30 kg/m2 were found to have an increased risk of ER+/PR+ breast cancer (RR=1.51, 95% CI: 1.24 - 1.85) and a reduced risk of ER-/PR- tumors (RR=0.62, 95% CI 0.40 - 0.96). Late age at first period (15 years versus 12 years old) (RR=0.72, 95% CI: 0.57 - 0.91), early age at first birth ( 20 years vs. nulliparous) (RR=0.69, 95% CI: 0.51 - 0.94), and increasing number of children (p trend <0.001) were found to be significantly associated with reduced risk only among those with ER+/PR+ tumors. Current use of postmenopausal estrogen only (ET) and estrogen-progestin combined therapy (EPT) both were found to be associated with increased risk of ER+/PR+ tumors (RR for ET=1.51, 95% CI: 1.16 - 1.97; RR for EPT=2.33, 95% CI: 1.97 - 2.75) and ER+/PR- (RR for ET=1.94, 95% CI: 1.09 - 3.44; RR for EPT=1.43, 95% CI: 0.97 - 2.12) tumors only. Consumption of alcohol was found to increase breast cancer risk for all ER/PR subtypes; compared to nondrinkers, women who drank at least two drinks per day had RRs varying from 1.5 to 2.6. Similarly, a family history of breast cancer was found to be associated with heightened risk of breast cancer independent of ER/PR status, with the RRs varying from 1.4 to 1.9.

Apigenin augments the growth inhibitory effects of doxorubicin in breast cancer cells derived from African American patients First AACR International Conference on the Science of Cancer Health Disparities, November 2007

The present study was designed to determine whether the flavonoid apigenin could suppress the growth of breast cancer cell lines derived from African-American breast cancer patients and whether apigenin would also augment the anticancer effects of doxorubicin (Adriamycin) in these cells. African-American women tend to develop breast cancer at a younger age and present with more aggressive, hormone-independent forms of the disease than women belonging to other ethnic groups in the U.S. Doxorubicin is widely used in chemotherapeutic regimens to treat breast cancer for all combinations of hormone receptor or p53 status. While patients with estrogen and progesterone receptor negative (ER-/PR-) breast cancer typically do derive benefit from doxorubicin, the onset of adverse side effects can significantly diminish their quality of life. Some patients use herbal supplements containing flavonoids while being treated with Doxorubicin, believing these products will potentiate its effectiveness. The cell lines included in the study included ER+/PR- HCC70 cells containing wild-type p53; ER-/PR- MDA-MB-468 cells containing mutant p53; and ER-/PR- HCC1806 and MDA-MB-157 cell lines that are p53 deficient. The ability of apigenin alone and in combination with doxorubicin to inhibit growth of these breast cancer cell lines was evaluated. Apigenin and doxorubicin each were found to reduce the growth of all the breast cancer cell lines, as determined by the Alamar BlueTM reduction assay. Apigenin was also found to potentiate the growth inhibitory and apoptotic effects of doxorubicin, as determined using phase-contrast microscopy and the Annexin V-PI assay. The authors conclude that apigenin might enhance the responsiveness of breast cancer patients to the anticancer effects of doxorubicin, including those with the more aggressive, hormone-independent forms of the disease.

ER+ PR- breast cancer defines a unique subtype of breast cancer that is driven by growth factor signaling and may be more likely to respond to EGFR targeted therapies Journal of Clinical Oncology, June 2006

The present study of tumors in women with operable breast cancer was designed to evaluate the role of the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor gefitinib (Iressa) in the treatment of breast cancer. Hormone receptor-based therapy has long been the mainstay for treatment of estrogen receptor positive (ER+) breast cancer. ER+/PR- disease is now known to exhibit different clinical behavior from ER+/PR+ disease. ER+/PR- disease has a lower response rate to estrogen deprivation, a worse prognosis compared to ER+/PR+ disease, and may be dependent on other signaling pathways. A total of 59 women were enrolled in the study, of which 43 proved to be suitable for molecular analysis. Frozen core biopsies were obtained from the women at baseline. The patients then received short-term exposure to gefitinib at least two weeks before surgery to remove the tumor, at which point a frozen tumor specimen was collected. The initial biopsies were classified according to the subtype of breast cancer (e.g. basal, luminal, HER2 amplified). To analyze the genetic changes caused by gefitinib, a direct comparison of the baseline sample and post-treatment tumor was performed. In addition, ER and PR status were determined. Of the 43 samples evaluated by microarray, 11 patients exhibited molecular growth inhibition in response to gefitinib, 10 patients demonstrated molecular growth proliferation, and 22 did not exhibit a significant change. When grouped by subtype, ER+/PR- and HER2 amplified tumors comprised a subgroup more likely to show molecular growth inhibition in response to gefitinib treatment. On the other hand, ER+/PR+ tumors were more likely to show molecular growth proliferation. The authors conclude that ER+/PR- breast cancer is growth factor dependent and constitutes a unique group of ER+ patients who may be more likely to benefit from EGFR inhibition.

Indole-3-carbinol-induced death in cancer cells involves EGFR downregulation and is exacerbated in a 3D environment Apoptosis, May 2006

The present study was designed to investigate indole-3-carbinol (I3C) induced cell death in several types of human breast cancer cells (MCF7, MDA-MB-468, MDA-MB-231 and HBL100) in comparison with normal fibroblasts. I3C, which is found in brassica vegetables such as broccoli, has been shown to inhibit breast cancer in animal models. Since epithelial cells are protected from cell death by a three-dimensional environment, 3D cell culture (collagen I gel and spheroids) was used to investigate the susceptibility of the cells to I3C. Cell viability in the presence of 256 μM I3C, which is a concentration close to the physiologically achievable range, was in the following order: fibroblasts = HBL100 > MDA-MB-231 > MCF7 > MDA-MB-468 in monolayer culture. However, in three-dimensional culture conditions, the susceptibility of MCF7 and MDA-MB-468 cancer cells to I3C was heightened. I3C caused cell death in MCF7, MDA-MB-468 and MDA-MB–231 cells via the mitochondrial apoptotic pathway. Further testing demonstrated that I3C-induced epidermal growth factor receptor reduction in these cells was likely to be responsible for the I3C-induced apoptosis.

The Relationship between Alcohol Use and Risk of Breast Cancer by Histology and Hormone Receptor Status Among Women 65–79 Years of Age Cancer Epidemiology, Biomarkers & Prevention, October 2003 Christopher I. Li, Kathleen E. Malone, Peggy L. Porter, Noel S. Weiss, Mei-Tzu C. Tang, Janet R. Daling

The current case-control study was designed to examine the relationship between alcohol consumption and the risk of the most hormonally-responsive breast cancer types (i.e., lobular or hormone receptor positive breast cancers). The study included 975 women 65 to 79 years of age diagnosed with invasive breast cancer during 1997–1999 in Washington State, as well as 1,007 controls. Ever-use of alcohol over the past 20 years was found to be associated with a 1.3-fold [95% confidence interval (CI), 1.0–1.5] increased risk of breast cancer, although this increase was mostly accounted for by women who drank at least 30.0 g per day of alcohol [OR, 1.7; CI: 1.1–2.6]. Ever-use of alcohol also was found to be associated with a 1.8-fold (CI: 1.3–2.5) increased risk of lobular cancer compared to a 1.2-fold (CI: 0.9–1.4) increased risk of ductal cancer. Ever-users of alcohol had an increase in risk of ER+/PR+ tumors (OR, 1.3; CI: 1.1–1.7), but no impact was observed for their risks of ER-/PR- or ER+/PR- breast cancer. The authors conclude that alcohol use appears to be more strongly associated with lobular and hormone receptor-positive cancers than it is with other types of breast cancer.

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