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In international comparisons and laboratory animal studies, diet has been shown to be one of the most consistent factors related to breast cancer etiology. In a large international study by Lahmann et al., 73,542 premenopausal and 103,344 postmenopausal women from multiple European countries, participating in the European Prospective Investigation into Cancer And Nutrition (EPIC) study were followed for 4.7 years; 1,879 incidents of invasive breast cancer were identified during this time period (Lahmann, Hoffmann, & Allen et al., 2004). The link between breast cancer and body size was modified by current hormone replacement therapy, especially among postmenopausal women. Also, among nonusers, risk for breast cancer was found to be strongly related with weight, body mass index (BMI) and hip circumference. Relative to normal women (BMI < 25), obese women were found to be at a 31% excess risk for breast cancer (Lahmann et al., 2004). Work in animal model systems implicates diet as important for affecting metastatic potential (National Academy of Sciences, 1989). In a study of 46 countries it was found that over 90% of breast cancer mortality could be accounted for mainly by dietary factors (Hebert & Rosen, 1996). The strongest protective effect was evident for cabbage, the most commonly consumed vegetable of the Brassica genus. One hypothesis is that this protective effect is due to its role in the modification of estrogen metabolism. This modification results in the metabolization of 17ï¢-Estradiol (E2) to 2-hydroxyestrone (2HE), instead of 16ï¡-hydroxyestrone (16HE): conferring a relatively lower cancer risk due to its interference with certain key biological mechanisms (Matthews, Fowke, & Dai et al., 2004). Multiple studies have shown that only tumor tissue contains Phase I enzymes, specifically CYP1B1 (McKay, Melvin, & Ah-See et al., 1995; Murray, Taylor, & McFadyen et al., 1997; Taylor, McKay, & Murray et al., 1996). Brassica vegetables contain high concentrations of indole glucosinolates that are converted to aryl hydrocarbon receptor agonists inside the body. These receptors can, in turn, cause the production of 2HE instead of 16HE as a result of E2 metabolism (Bjeldanes, Kim, & Grose et al., 1991; Michnovicz & Bradlow, 1991; Kall, Vang, & Clausen, 1996).
INTRODUCTION TO MALE BREAST CANCER
Male breast cancer is relatively rare, especially when compared to female breast cancer (Giordano, Cohen, & Buzdar et al., 2004). According to the American Cancer Society, in the United States, invasive breast cancer was diagnosed in approximately 1,910 men in 2009. Approximately 440 American men died as a result of breast cancer in 2009 (American Cancer Society, 2010). Male breast cancer is possible because most men have at least some breast tissue and, like any other cells of the body, the cells of this breast tissue may undergo carcinogenesis and be transformed into cancer cells. The breast consists of lobules, the glands that produce milk; ducts, the tubes that transport milk produced by the lobules to the nipple; and stroma, tissues around the lobules and ducts (American Cancer Society, 2010). Before puberty, both males and females have a small amount of breast tissue. However, just after puberty, the breast tissue of females starts to grow, whereas, the breast tissue of males' stops growing. These changes in breast development occur due to the production of female and male sex hormones beginning at puberty. In females, the female sex hormones trigger the development of breast tissue. In males, the male sex hormones stop the development of breast tissue. Thus, it can be reasoned why male breast cancer is relatively rare when compared to female breast cancer. First, the breast tissue of males is less developed than the breast tissue of females. Second, unlike the breast tissue of females, the breast tissue of males is not exposed to the growth enhancing effects of large amounts of female sex hormones (American Cancer Society, 2010).
The risk factors for male breast cancer include old age, male or female relatives with breast cancer, alcohol consumption, inheritance of BRCA1, BRCA2, CHEK2 and PTEN gene mutations, Klinefelter's syndrome, exposure to radiation, liver disorder, lack of physical activity, obesity, and estrogen treatment (Strong, Yarber, & Sayad et al., 2006). The symptoms of male breast cancer include swelling of the breast, nipple discharge, dimpling of the skin, retraction of the nipple, and reddening of the breast skin. The diagnosis of male breast cancer involves mammography, ultrasound, clinical breast examination, nipple discharge examination, and biopsy (Strong et al., 2006). The major treatment options for male breast cancer include chemotherapy, radiation therapy, and surgery.
ADVANCES IN BREAST CANCER RESEARCH
The Southern region of the United States is unique for having a strong relationship between physical activity and degree of urbanization. Here, unlike any other region, African Americans tend to reside in rural areas as opposed to being urban dwellers like their counterparts in other regions (Centers for Disease Control and Prevention, 2003). For instance, data from the Behavioral Risk Factor Surveillance System indicate that 53.8% of South Carolinians do not meet recommended moderate physical activity guidelines. This is accounted for primarily by 63.3% African Americans followed by 57.1% Hispanics and 51.1% European Americans. Factors associated with lower levels of recommended physical activity include those of low socioeconomic status (SES) and season (Brownson, Eyler, & King et al., 2000; Jones, Ainsworth, & Croft et al., 1998; Dannenberg, Keller, & Wilson et al., 1989; Levin, Jacobs, & Ainsworth et al., 1999; Matthews, Freedson, & Hebert et al., 2001). When compared to urban dwellers, rural residents are more likely to have a relatively lower SES. Also, seasonal environment changes may present various obstructions for physical activity. Physical inactivity was measured at 43.1% amongst the most rural Southern residents as opposed to 26.7% for the most urban dwellers. This is contradictory to the results obtained from the other regions of the United States that show a similarity in physical inactivity among the urban residents, however, substantially lower physical inactivity for the rural residents: West - 19.7%, Northeast - 26.3% and Midwest - 28.4% (Centers for Disease Control and Prevention, 2003). Southern rural European American and African American residents account for relatively higher physical inactivity (38%, 39% respectively) when compared to their urban counterparts (24%, 32% respectively). Conversely, rurally residing Hispanics accounted for less than half the physical inactivity (19%) than for the urban residing ones (40%). The highest physical activity in the South was among the urban dwellers (28.7%) and lowest for the most rural residents (15.4%) (Martin et al., 2005). Hence, the odds for rural residents meeting the physical activity recommendation relative to their urban equal is 0.46.
Highly reproducible and dose-dependent inhibition of experimentally induced breast cancer has been produced by dietary energy restriction (DER), as shown by the results from preclinical models. Mammary carcinogenesis is inhibited by physical activity; however, it's not known whether these effects depend on energy balance. It has been shown by emerging data that increased amount of corticosterone and reduced amount of insulin-like growth factor (IGF-1) may be associated in the DER-mediated protection against breast cancer; nevertheless, an increased amount of IGF-1 may be produced under conditions of physical activity (Thompson, Zhu, & Jiang, 2004). Hence, there is a need for more research in to the equivalence of physical activity, DER and their combination in breast cancer prevention under comparable conditions of energy balance. Also, reduction in BMI along with higher levels of physical activity, and lower caloric consumption may provide support for clinical trials evaluating insulin level change and breast cancer risk by lowering insulin levels (Chlebowski, Pettinger, & Stefanick et al., 2004). Due to the presence of relatively few studies documenting weight loss among African American women and the absence of a weight loss/breast health combined intervention, Fitzgibbon et al. conducted a randomized intervention trial for studying the feasibility of a combined weight loss/breast health intervention for 64 overweight or obese African American women. The project was executed in two cohorts with high retention for both. However, only Cohort 2 was observed to decrease body weight, increase the frequency of physical activity, and decrease the consumption of dietary fat relative to the control group. Nevertheless, both cohorts showed increased proficiency in breast self-examination relative to the control group (Fitzgibbon, Stolley, & Schiffer et al., 2005).
To study the relationship between risk of breast cancer and consumption of dietary lignan, McCann et al. conducted a population-based case-control study. It was found that specifically for premenopausal women dietary lignans may be important in the etiology of breast cancer. Reduced risk of breast cancer was observed among premenopausal women in the highest quartile of dietary lignan consumption. On the other hand, for postmenopausal women, no relationship was found between risk of breast cancer and dietary lignan consumption (McCann, Muti, & Vito et al., 2004).
The importance of total energy consumption in breast cancer risk has been shown through laboratory animal studies. When compared to overall energy consumption, the effect of fat was found to be relatively weak in the examination of the independent effects of fat and energy consumption on breast cancer in animal studies. The consumption of fat has been shown to decline for the past several years by the surveys designed to measure actual individual consumption. In comparison to normal US women, despite the relatively small amounts of animal products consumed by Seventh-Day Adventists, the breast cancer rates for Seventh-Day Adventists are only slightly lower than the other US women. Furthermore, when compared to single women from the general population, no meat eating UK nuns had breast cancer rates very similar to the single women (Holmes & Willet, 2004).
Ursin et al. conducted a multicenter case-control study to examine the relationship between risk of breast cancer in both African American and European American women and reproductive factors. This study revealed that there was a 13% reduction in risk per full-term pregnancy in European American women aged 35 to 49 years and 10% reduction in risk for those aged 50 to 64 years. These figures were 10% and 6%, respectively, for African American women. For all women, the number of full-term pregnancies were directly related to a substantial reduction in risk. However, for younger European American and African American women who had already given birth an inverse relationship was found between risk of breast cancer and duration of lactation (Ursin, Bernstein, & Wang et al., 2004).
Whiteman et al. conducted a population-based study to examine the relationship between certain reproductive factors and mortality in 4,299 U.S. women diagnosed with breast cancer. The follow-up of approximately 14.5 years revealed 1,847 deaths. Women who had last given birth less than twelve months ago and were also diagnosed with breast cancer had an increased mortality risk relative to women who had never given birth. There was a 65% survival rate for 15 years among women who had never given birth and 38% survival rate for women who had last given birth less than 12 months ago. Hence, according to this study, for women diagnosed with breast cancer a recent birth may be an unfavorable prognostic indicator (Whiteman, Hillis, & Curtis et al., 2004).
Women, who breast-feed for a cumulative total of more than 1 year while having deleterious BRCA1 mutations, have been found to have a significantly reduced risk of breast cancer than those who never breast-fed (Jernstrom, Lubinski, & Lynch et al., 2004). Mammography screening efficiency and effectiveness has been found to be lower for users of hormone replacement therapy relative to non-users (Banks, Reeves, & Beral et al., 2004). The process by which Steroid Hormone Receptors (SHRs) regulate gene expression, and the interaction of SHRs with other biological pathways has been started to be clarified. The downstream functions of SHRs may eventually provide additional therapeutic targets (Ko & Balk, 2004).
To study the relationship between the amount of sex hormones and risk of breast cancer, Zeleniuch-Jacquotte et al. conducted a case-control study. The results of this study indicated that there is no statistically significant relationship between the amount of sex hormones and risk of breast cancer (Zeleniuch-Jacquotte, Gu, & Shore et al., 2005). Studies have revealed that the addition of testosterone to the estrogen-progestin treatment plan can potentially decrease the stimulating effects of these hormones on breast tissue. However, due to the potential risk of enhanced aromatization to estrogen in this case, testosterone therapy cannot be recommended by itself for estrogen deplete women. In addition, greater amount of testosterone has been linked with higher risk of breast cancer among postmenopausal women, who are estrogen deplete and have increased adipose aromatase activity (Somboonporn & Davis, 2004).
Health care practitioners in the UK tend to preferentially prescribe tibolone for hormone replacement therapy of increased breast cancer risk women or women with long-term history of being prescribed estrogen-only therapy; with other combination products being prescribed for normal women. Hence, the prescription received is usually dependent on the clinical background of the women (Wierik, Hendricks, & Boerstoel-Streefland, 2004). Hormone replacement therapy is not a direct cause of breast cancer; instead there are sequences of mutations that must occur in order to develop invasive breast cancer. The only association between hormone replacement therapy and increased diagnosis of breast cancer is due to the promotion of an existing oncogenic change, and not due to sex hormones initiating malignant mutations. In essence, sex hormones have mutagenic properties but they are generally not oncogenic (Wren, 2004).