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Minggu, 17 Juni 2018

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Risk factors for breast cancer can be divided into preventable and unavoidable. Their studies are included in the epidemiological field. Breast cancer, like other forms of cancer, can result from various environmental and hereditary risk factors. The term "environment", as used by cancer researchers, means any risk factors that are not genetically inherited.

For breast cancer, the list of environmental risk factors includes individual individual development, microbial exposure, "medical intervention, food exposure for nutrients, energy and toxins, ionizing radiation, and chemicals from industrial and agricultural processes and from consumer products... reproduction options, energy balance, adult weight gain, body fatness, voluntary and unintentional physical activity, medical treatment, exposure to tobacco smoke and alcohol, and occupational exposure, including shift work "as well as" metabolic and physiological processes that alter the internal body of the environment. " Some of these environmental factors are part of the physical environment, while others (such as diet and number of pregnancies) are a major part of the social, cultural, or economic environment.

Although many epidemiological risk factors have been identified, the cause of any breast cancer is most often unknown. Epidemiological studies inform the pattern of occurrence of breast cancer in certain populations, but not in certain individuals. About 5% of new breast cancers are due to hereditary syndrome, and established risk factors account for about 30% of cases.


Video Risk factors for breast cancer



Age

The risk of developing breast cancer increases with age. A woman is more than 100 times more likely to develop breast cancer in her 60s than in her 20s. If all women live to age 95, about one in eight will be diagnosed with breast cancer at some point during their lifetime. However, the actual lifetime risk is lower than that, as 90% of women die before the age of 95, most commonly from heart attacks, strokes, or other forms of cancer.

Breast cancer probability increases with age, but breast cancer tends to be more aggressive in younger people.

Maps Risk factors for breast cancer



Sex

Individual males have a lower risk of developing breast cancer than women. In developed countries, about 99% of cases of breast cancer are diagnosed in female patients; in some African countries, representing the highest incidence of male breast cancer, men accounted for 5-15% of cases. The rate of male breast cancer appears to be increasing.

Male breast cancer patients tend to be older than females. They are more likely to be diagnosed with hormone-receptor positive tumors, with about six of seven cases of positive estrogen-receptor. The overall prognosis is worse for men than for female patients.

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Heredity

The United Kingdom, which is a member of the International Cancer Genome Consortium, led efforts to map the complete genome of breast cancer.

BRCA1 and BRCA2

In 5% of cases of breast cancer, there is a strong family inherited risk.

Two autosomal dominant genes, BRCA1 and BRCA2 , are the most common cause of familial breast cancer. Women carrying harmful BRCA mutations have a 60% to 80% risk of breast cancer in their lives. Other associated malignancies include ovarian cancer and pancreatic cancer. If a mother or sister is diagnosed with breast cancer, the risk of gene mutation BRCA1 or BRCA2 is about 2 times higher than women who do not have a family history. Commercial tests for the gene mutations BRCA1 and BRCA2 have been available in most developed countries since at least 2004.

In addition to the BRCA genes associated with breast cancer, the presence of NBR2 , near the breast cancer gene 1, has been found, and studies in its contribution to the pathogenesis of breast cancer are ongoing.

Other genes

Non-BRCA1 and non-BRCA2 breast tumors (and even some sporadic carcinomas) are believed to result from weak penetration expressions but very common mutations in various genes. For example, polymorphisms have been identified in genes associated with estrogen metabolism and/or carcinogens (Cytochrome P450, family 1, member A1, CYP1B1, CYP17A1, CYP19, Catechol-O-methyl transferase, N-acetyltransferase 2, Glutathione S- transferase Mu 1 , GSTP1, GSTT,...), for the action of estrogens, androgens and vitamin D (ESR1, AR, VDR), for the mutual activation of gene transcription (AIB1), to DNA damage response pathways (CHEK2, HRAS1, XRCC1, XRCC3, XRCC5 ). These gene sequence variants that are relatively common in the population may be associated with a relatively small to moderate increase in risk for breast cancer. The combination of these variants can cause multiplication effects. Sporadic cancer is probably the result of a complex interaction between low penetration gene expression ( risk variant ) and environmental factors. However, the alleged impact of most of these variants on the risk of breast cancer should, in many cases, be confirmed in large population studies. Indeed, low penetration genes can not be easily traced through the family, just as dominant genes are high risk.

Part of non-BRCA1 and non-BRCA2 breast tumors may be associated with a rare syndrome, in which breast cancer is only one component. Such syndromes result mainly from mutations in TP53 (Li-Fraumeni syndrome), ATM (Ataxia Telangiectasia), STK11/LKB1 (Peutz-Jeghers syndrome), PTEN (Cowden syndrome).

RAB11FIP1, TP53, PTEN and rs4973768 were also associated with an increased risk of breast cancer. rs6504950 is associated with a lower risk of breast cancer.

Mutations in RAD51C provide an increased risk for breast and ovarian cancers.

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Previous cancer

People who have previously been diagnosed with breast, ovarian, uterine, or colon cancers have a higher risk of developing breast cancer in the future. Mothers of children with soft tissue sarcomas may have an increased risk of breast cancer. Men with prostate cancer may have an increased risk of breast cancer, although the absolute risk remains low.

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Food factor

Alcohol

In a population study that did not control for screening incidents of alcohol drinkers had a higher tendency to be diagnosed with breast cancer. For example, a study of more than one million middle-aged women in the UK concluded that every alcoholic beverage each day was associated with 11 cases of breast cancer incidence per 1,000 women. This means that among a group of 1000 women who drink one alcohol per day, they will have an additional 11 cases of breast cancer when compared to a group of women who drink less than one alcoholic beverage per week; a group of 1000 women who have four drinks per day will have an additional 44 cases of breast cancer compared with non-drinkers. One or two drinks a day increases the relative risk up to 150% from normal, and six drinks per day increases the risk up to 330% from normal.

However, studies of mortality indicate that drinkers do not have a greater risk of death from breast cancer. Analysis of various causes of death of elderly and elderly Americans found that of 251,420 women in the study, 0.3% of zero and super-bright drinkers died of breast cancer, during 10 years of research. And the exact same proportion, 0.3%, from moderate to heavy drinkers (1 to 4 drinks per day). In another mortality study of 85,000 women, the chances of dying from breast cancer during 12 years of follow-up were 0.4%, and again this is identical for zero-to-super-light drinkers such as moderate to severe drinkers. This paradoxical difference between outcomes for diagnosis and mortality appears to be due to drinkers who do more screening for reasons of breast cancer because higher screening rates among drinkers are because they are richer, more urbanized, more health conscious, closer to the clinic screening.. Studies that control for screening rates indicate no association between drinking and being diagnosed with breast cancer.

Meta-analysis of epidemiological studies looking at drinking and breast cancer death/survival after diagnosis showed no association between drinking levels (before or after diagnosis) and risk of breast cancer death, or recurrence of cancer. Two recent studies looking at patients already diagnosed with breast cancer both found that women who drank prior to their breast cancer diagnosis did not have a higher risk of dying from cancer than non-drinkers. Similarly, a large study with long follow-up of women with breast cancer suggests breast cancer patients have a better chance of survival if they are regular drinkers before diagnosis. If they change their drink after diagnosis, this does not change their chances of dying from breast cancer. But increased drinking was associated with an overall increase in overall life expectancy (primarily because of the deaths of much less heart disease among those who increased their alcohol consumption).

Fat intake

The effects of food have been examined for decades with conflicting results and so far failed to confirm a significant relationship. One recent study shows that a low-fat diet can significantly reduce the risk of breast cancer and breast cancer recurrence. Another study showed no contribution of fat intake in the incidence of breast cancer in more than 300,000 women. A randomized, controlled study on the consequences of a low-fat diet, conducted as part of the Women's Health Initiative, failed to show a statistically significant reduction in the incidence of breast cancer in the low-fat diet group, although the authors did find evidence of the benefits in female subgo- nals who follow a low-fat diet strictly. A prospective cohort study, Nurses' Health Study II, found an increased incidence of breast cancer in premenopausal women only, with higher animal fat intake, but not vegetable fat. Overall, these results indicate a possible association between dietary fat intake and breast cancer incidence, although this interaction is difficult to measure in a large group of women.

Food-specific fatty acids

Although many claims have been made in the popular literature there is no compelling evidence linking specific fats with breast cancer.

A study published in 2001 found a higher level of monounsaturated fatty acid MUFA (especially oleic acid) in the postmenopausal female erythrocyte membrane that developed breast cancer.

That same study discusses that a diet high in MUFAs is not a major determinant of erythrocyte membrane MUFAs, in which most oleic acid in mammalian tissues comes from saturated stearate acid residues. Where the key conversion is controlled by Delta9-desaturase, which also regulates the transformation of other common saturated fatty acids (SFA) (myristic and palmitate). This study discusses that dietary fat content has important effects on Delta9-d activity, while high levels of SFA increase Delta9-d activity by up to three-fold, while polyunsaturated fatty acids (PUFAs) decrease.

This conclusion is partially contradicted by recent studies, which show a direct relationship between the consumption of omega-6 fatty acids (PUFAs) and breast cancer in postmenopausal women.

Phytoestrogen

Phytoestrogens have been extensively studied in animals and in-vitro and epidemiological studies. Research fails to find any real benefits and some phytoestrogens can pose a risk of breast cancer.

The literature supports the following conclusions:

  1. The intake of plant estrogen in early adolescence can protect against breast cancer later in life.
  2. The potential risk of isoflavones in breast tissue in women at high risk of developing breast cancer remains unclear.

Calcium

Several studies have found an association between calcium intake and reduced risk of breast cancer.

  • In Nurse Health Study, intake of high calcium foods showed a 33% lower risk of breast cancer.
  • Cancer Prevention Study II Nutrition Group Concluded 20% lower risk of breast cancer with 1250 mg calcium intake.
  • Women's Health Studies show an inverse relationship between total calcium intake and risk of premenopausal breast cancer.
  • Two other studies, one in France and one in Finland, show a significant inverse relationship between calcium intake and breast cancer.
Hypothesis
  • Calcium reduces cell proliferation and induces differentiation in the mammary gland.
  • A high intake of calcium reduces epithelial hypoproliferation caused by glandular fat and chemically induced carcinogenesis.
  • Breast density is positively associated with breast cancer. Food calcium intake reduces breast density.
  • High calcium intake is associated with a reduced risk of benign benign epithelial disorder that is considered a precursor of breast cancer.

Vitamin D

Vitamin D is associated with a decreased risk of breast cancer and disease prognosis. A 2011 study conducted at the University of Rochester Medical Center found that low vitamin D levels among women with breast cancer were correlated with more aggressive tumors and a worse prognosis. This study correlates less optimal levels of vitamin D with poor scores on every major biological marker that helps doctors predict patient breast cancer outcomes. The lead researcher stated, "Based on these results, doctors should strongly consider monitoring vitamin D levels among breast cancer patients and correcting them as needed."

Hypothesis
  • Vitamin D (25 (OH) D, 1, 25 (OH) 2 D) metabolites promote cellular differentiation and are important for chemoprevention.
  • The low circulating levels of 25 (OH) D in adolescents can be an important predisposing factor for later breast cancer risk.

Brassica Vegetables

In a study published in the Journal of the American Medical Association, biomedical researchers found that intake of Brassicas vegetables (broccoli, cauliflower, cabbage, kale and Brussels sprouts) was inversely proportional to the development of breast cancer. The relative risk among women in the highest decile consumption of Brassica vegetables (median, 1.5 servings per day) compared with the lowest decile (almost no consumption) was 0.58. That is, women who consumed about 1.5 servings of Brassica vegetables per day had a 42% less risk of breast cancer than those who barely consume at all.

Country diet

Significant environmental effects are most likely responsible for different rates of breast cancer incidence across countries with different eating habits. Researchers have long measured that breast cancer rates in immigrant populations soon became similar to host country levels after several generations. The reason for this is to speculate on becoming a connoisseur of the host country diet. A prototypical example of this phenomenon is the change in breast cancer rates after the arrival of Japanese immigrants to America.

Mushroom

In 2009, a case-control study of the 2,018 female eating habits suggested that women who consumed the fungus had a 50% lower incidence of breast cancer. Women who consumed mushrooms and green tea had a 90% lower incidence of breast cancer. A case-control study of 362 Korean women also reported an association between yeast consumption and reduced risk of breast cancer.

iodine deficiency

The protective effect of iodine on breast cancer has been postulated from epidemiological evidence and described in animal models.

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Obesity and Lack of Exercise

Gaining weight after menopause can increase a woman's risk. A 2006 study found that taking 9.9 kg (22 pounds) after menopause increased the risk of breast cancer by 18%. Lack of exercise has been linked to breast cancer by the American Institute for Cancer Research.

Obesity has been linked to an increased risk of developing breast cancer by many scientific studies. There is evidence to suggest that excess body fat at the time of breast cancer diagnosis is associated with higher rates of cancer recurrence and mortality. Furthermore, studies have shown that obese women are more likely to have large tumors, greater lymph node involvement, and a worse prognosis of breast cancer with a 30% higher mortality risk.

Weight gain after diagnosis is also associated with higher rates of recurrence or breast cancer death despite these inconsistent findings. Weight gain is often less severe with newer chemotherapy treatments but one study found a significant risk of breast cancer death in women who gained weight compared to those who maintained their weight. However, other cohort studies and recent clinical trials have not shown a significant relationship between weight gain after diagnosis and breast cancer death.

Weight loss after diagnosis has not been shown to reduce the risk of breast cancer recurrence or death. However, physical activity after the diagnosis of breast cancer has shown some association by reducing breast cancer recurrence and death independent of weight loss. Data for both weight loss and physical activity and effects on the prognosis of breast cancer are lacking.

There is a debate as to whether higher breast cancer rates associated with obesity are due to biological differences in cancer itself, or differences in other factors such as screen health practices. It has been suggested that obesity can be a determinant for breast cancer screening by mammography. Seventeen scientific studies in the United States have found that when obesity increases in women over 40 years, mammography rates are reported to decrease significantly. When grouped by race (white vs black) there is a stronger relationship between obesity and lack of mammography screening among white women. Other studies have also found lower levels of mammography among those who are overweight and obese than women with normal body mass index - this effect is seen only in white women. Overweight women are more likely to list pain relating to mammograms as an excuse not to be screened; However, leaner women also include this as an excuse to avoid mammograms. Another reason fat women can avoid mammography is due to lack of insurance, low income, or embarrassment to the procedure, although when these factors are accounted for, the effect of lower screening rates is still significant. In contrast, other studies have shown that mammography patterns do not differ among women who are obese compared with those with healthy weight indicating that there may be biological differences in cancer presentations between these groups.

Hormones

Increased levels of estrogen in the blood are continuously associated with an increased risk of breast cancer, such as elevated levels of androgens androstenedione and testosterone (which can be altered directly by aromatase to estrogen estrone and estradiol). Increased levels of progesterone in the blood is associated with a decreased risk of breast cancer in premenopausal women. A number of conditions that increase endogenous estrogen exposure include not having children, delaying the first birth, not breastfeeding, early menarche (first menstrual period) and late menopause suspected to increase lifetime risk for developing breast cancer.

However, not only sex hormones, but also insulin levels are positively associated with breast cancer risk.

Pregnancy, childbirth and breastfeeding

The lower age of first birth, compared with the median age of 24 years, had more children (about 7% lower risk per child), and breastfeeding (4.3% per year of breastfeeding, with an average relative risk of about 0 , 7) are all correlated to lower risk of breast cancer in premenopausal women, but not postmenopausal women, in large studies. Women who give birth and breastfeed at age 20 may have greater protection. Conversely, for example, having a first live birth after age 30 doubled the risk compared to having a first live birth at less than 25 years of age. Never have children tripled the risk. Studies have found that these risk factors become less material when a woman reaches menopause, that is, they affect the risk of breast cancer before menopause but not afterwards. In balancing premenopausal reductions in the risk of labor and breast-feeding, it is also important to consider the risks involved in having children.

Hormonal contraceptives

Hormonal contraceptives can produce a slightly increased risk of breast cancer diagnosis among current and recent users, but this appears to be a short-term effect. In 1996, the largest collaborative analysis of individual data on more than 150,000 women in 54 breast cancer studies found a relative risk (RR) of 1.24 breast cancer diagnoses among current oral contraceptive pill users; 10 years or more after quitting, there is no visible difference. Furthermore, cancer diagnosed in women who have used advanced hormonal contraceptives compared with nonusers, increases the likelihood that small advantages among users are due to increased detection. The relative risk of breast cancer diagnosis associated with current and recent use of hormonal contraceptives does not seem to differ from the family history of breast cancer. Several studies have shown that women who start using hormonal contraceptives before the age of 20 or before their first full pregnancy on an increased risk of breast cancer, but it is unclear how many risks come from early age on first use, and how many stems are used before the first full pregnancy.

Hormone replacement therapy

Data exist from both observational and randomized clinical trials regarding the relationship between menopausal hormone replacement therapy (HRT menopause) and breast cancer. The largest meta-analysis (1997) data from 51 observational studies, showed a relative risk of breast cancer 1.35 for women who had used HRT for 5 years or more after menopause. The estrogen-plus-progestin arm of the Women's Health Initiative (WHI), a randomized controlled trial, which randomized more than 16,000 postmenopausal women to receive joint hormone therapy or a placebo, was stopped early (2002) because health risks outweighed benefits. One of the adverse results leading to closure was a significant increase in total and invasive breast cancer (hazard ratio = 1.24) in women who randomly received estrogen and progestin for an average of 5 years. HRT-associated breast cancers have adverse prognostic characteristics (advanced stages and larger tumors) compared with cancer occurring in the placebo group, and HRT is also associated with a substantial increase in abnormal mammograms. The use of short-term hormones for the treatment of menopausal symptoms seems to give little or no risk of breast cancer. Correlation was found between the use of hormonal contraceptives and subsequent dependence on hormone replacement therapy.

Oophorectomy and mastectomy

Prophylactic oophorectomy (removal of the ovaries) and mastectomy in individuals with high-risk mutations of BRCA1 or BRCA2 genes reduce the risk of developing breast cancer and reduce the risk of ovarian cancer. Due to the complex balance of benefits and risks of prophylactic surgery, it is recommended only in very specific cases.

Hormonal therapy

Hormonal therapy has been used for chemoprevention in individuals who are at high risk for breast cancer. Overall it is recommended only in very special circumstances. In 2002, clinical practice guidelines by the US Preventive Services Task Force (USPSTF) recommended that "doctors discuss chemoprevention with women at high risk for breast cancer and are at low risk for adverse effects of chemoprevention" with recommendation level B. Selective_estrogen_receptor_modulators_ (SERMs) "> Selective estrogen receptor modulators (SERMs)

These guidelines are based on the SERM study of MORE, BCPT P-1, and Italian trials. In the MORE TESTS, the relative risk reduction for raloxifene was 76%. Prevention studies of P-1 show that tamoxifen can prevent breast cancer in high-risk individuals. Relative risk reduction of up to 50% of new breast cancers, although cancer is prevented is more likely to be positive for estrogen receptors (this is analogous to the finasteride effect on prostate cancer prevention, where only low-level prostate cancer is prevented). Experiments in Italy show the benefits of tamoxifen.

Additional randomized controlled trials have been published since the guidelines. The IBIS trial found the benefits of tamoxifen. In 2006, the NSABP STAR trial showed that raloxifene has the same efficacy in preventing breast cancer compared with tamoxifen, but that there are fewer side effects with raloxifene. The RUTH trial concluded that "the benefits of raloxifene in reducing the risk of invasive breast cancer and vertebral fractures should be weighed against an increased risk of venous thromboembolism and fatal stroke". On September 14, 2007, the US Food and Drug Administration approved raloxifene (Evista) to prevent invasive breast cancer in postmenopausal women.

Endocrine disruptors

Many xenoestrogens (industrial-made estrogenic compounds) and other endocrine disruptors are potential risk factors for breast cancer.

Diethylstilbestrol (DES) is a synthetic form of estrogen. It has been used between the early 1940s and 1971. Pregnant women take DES to prevent certain pregnancy complications. However, it also increases the risk of breast cancer. It also increases the risk of breast cancer in prenatally affected girls after they reach the age of 40 years.

Furthermore, there is exposure to endocrine disruptors from the environment, in addition to the above mentioned phytoestrogens in the diet section. See xenoestrogens in environmental factors below


Factors in the physical environment

According to a review, the main mechanism by which environmental compounds increase the risk of breast cancer acts like hormones, especially estrogen, or affects susceptibility to carcinogenesis. The evidence to date generally supports the link between breast cancer and aromatic polycyclic hydrocarbons (PAHs) and polychlorinated biphenyls (PCBs). Dioxins and organic solvents, on the other hand, exhibit only limited and limited methodological research, but are suggestive of associations. Overall, however, evidence remains based on relatively small studies.

Xenoestrogens

Many xenoestrogens (industrial-made estrogenic compounds) are endocrine disruptors, and potential risk factors for breast cancer. Endocrine disorders are the hypothesis that some chemicals in the body, such as Bisphenol A, can interfere with the production, processing, and transmission of hormones.

Substantial and growing evidence suggests that exposure to certain toxic chemicals and hormone coping compounds including chemicals used in pesticides, cosmetics and cleaning products contributes to the development of breast cancer.

The increased prevalence of these substances in the environment can account for the increased incidence of breast cancer, although direct evidence is rare.

Bisphenol A

Bisphenol A (BPA) is a chemical compound used in the production of plastics found in various commercial products, including laptops, baby bottles, food containers, water pipes, and laboratory equipment and hospitals. BPA was first produced in 1891, but its estrogenic properties had not been discovered until the mid-1930s. Today it is considered as xenoestrogen, and serves as an endocrine disrupter that disrupts hormones in the body and disrupts the normal functioning of the endocrine system. At very low levels, the FDA has long considered BPA in food to be safe, but it has been challenged for years because more information is being discovered about the effects of chemicals.

Prenatally affected mice for environmentally relevant BPA doses show an increase in the number of intraductal hyperplasia (precancerous lesions) in the mammary glands that appear during adulthood, while high doses induce development of carcinoma in breast tissue. Animals exposed to BPA during fetal life develop a palpable tumor, and all studies show an increased susceptibility to mammary gland neoplasia that manifests during adulthood. Exposure to mammary dams to the environmentally relevant BPA levels during organogenesis results in major changes in the mammary gland. It was concluded that perinatal exposure to low doses of BPA resulted in changes in mammary gland morphogenesis, induction of precancerous lesions, and in situ carcinoma.

A study attempted to determine whether early exposure to BPA could accelerate the carcinogenesis of mammas in dimethylbenzanthracene (DMBA) models of rodent mammary cancer. In the study, the scientists exposed neonatal/prebubertal mice to BPA through lactation of oral nursing dams given orally with 0, 25, and 250 Âμg BPA/kg body weight/day. For the study of tumorigenesis, female offspring were exposed to 30 mg DMBA/kg body weight at 50 days of age. DMBA induces breast tumors and allows the predisposing chemicals for breast cancer to increase the amount of mammary adenocarcinoma. The results showed that female rats in the control group, BPA 25, and BPA 250 given the DMBA showed an increase that relied on BPA doses on mammary tumors. Each group had 2.84, 3.82, and 5.00 breast tumors per mouse. Treatment with BPA also reduced tumor latency, with mean tumor latency averages of 65, 53, and 56.5 days for group 0, BPA 25, and BPA 250 respectively. Maternal exposure to BPA during breastfeeding decreased time for first tumor latency and increased the number of DMBA-induced mammalian tumors in female offspring. If these effects are found in rodents carried to humans, even minimal exposure to BPA can lead to an increased risk for breast cancer.

Increased breast cancer incidence in women has been associated with prolonged exposure to high estrogen levels. Xenoestrogens, like BPA have the capacity to disrupt normal hormonal actions. This study provides evidence of the estrogenic effects of BPA. In this study human breast epithelial cells MCF-10F treated with 10-3 M, 10-4 M, 10-5 M and 10-6 M BPA continuously for two weeks. Cells treated with 10-3 M BPA died on the second day of treatment. Concentrations of 10-4 M BPA are also toxic to breast epithelial cells, and they die on the fourth day of treatment. These data suggest that this BPA concentration is toxic to MCF-10F cells. After a two-week observation period, it appears that the cells form a high percentage of channels such as structures in collagen. MCF-10F cells treated with 10-5 M and 10-6 M BPA formed a high percentage of solid mass, 27% and 20%, respectively. These data suggest that BPA is capable of inducing neoplastic transformation of human breast epithelial cells. Epigenetic changes are involved in the early stages of initiation of cancer by altering the ductulogenesis. BPA is able to induce the transformation of MCF-10F human breast epithelial cells. After treatment with BPA, cells produce fewer collagen tubules and more dense masses.

Consumer groups recommend that people who want to lower their exposure to bisphenol A avoid canned food and polycarbonate plastic containers (which share resin identification code 7 with many other plastics) unless the packaging shows the plastic is bisphenol A-free. The National Toxicology Panel recommends avoiding microwaved food in plastic containers, inserting plastic into dishwashers, or using hard detergent on plastics, to avoid washing.

Aromatic Amines

Aromatic amines are chemicals produced when products like dyes, polyurethane products, and certain pesticides are made. They are also found in cigarette smoke, fuel exhaust, and cooked meat. Three types of monocyclic aromatic amines, polycyclic, and heterocyclic have all been found in recent studies on breast health. Monocyclic amines have been found to cause breast cancer in mice. Studies have shown that women who eat higher amounts of cooked meat, which means more exposure to heterocyclic amines, have also been diagnosed with post-menopausal breast cancer. Heterocyclic amines also have the ability to mimic estrogen and in laboratory studies have been found to promote the growth of cancerous tumors in human tissues.

Benzene

Benzene is a petrochemical solvent. Benzene exposure mostly comes from air pollution resulting from industrial combustion, exhaust and gas fumes, and cigarette smoke. Petroleum, distillates such as gasoline, car and truck exhaust also contain benzene. The International Agency for Research on Cancer and the National Toxicology Program has labeled benzene as a definite human carcinogen. Several studies have shown a correlation between benzene exposure and breast cancer risk. Laboratory studies in mice have shown that high exposure to benzene can cause breast cancer.

DDT

Although DDT pesticides were banned more than 20 years ago, studies have shown that there are still trace amounts found in certain agricultural products, as well as in human and animal milk. While individual studies have come to conflicting conclusions, recent reviews of all evidence suggest that DDT exposure before puberty increases the risk of breast cancer later in life.

Ethylene oxide

Ethylene oxide is a chemical that can be found in some personal care products, especially in the form of aromas. It is also used for the sterilization of various medical objects. The National Toxicology Program has labeled ethylene oxide as a definite human and animal carcinogen. A study conducted by the National Institute for Occupational Safety and Health including 7,576 women found a direct correlation between breast cancer rates and exposure to ethylene oxide during the medical sterilization process. Also, human breast cells that come into contact with a small amount of ethylene oxide in the laboratory can cause DNA damage to the breast tissue.

Polycyclic aromatic hydrocarbons

Polycyclic aromatic hydrocarbons are chemical products of combustion from coal burners, fuel, cigarette smoke, and various other sources. PAHs are often found in the air and inhaled into the body. PAH bioaccumulates easily and can copy the hormone estrogen. PAHs can also be genotoxic, meaning they have the ability to damage DNA.

Vinyl chloride

Vinyl chloride is produced when PVC or polyvinyl chloride is made. PVC is found in plastic packaging, outerwear, plastic toys and other plastic products. Vinyl chloride can be found in cigarette smoke and air around the garbage and the soil is filled. It can also be found in wastewater when PVC is made. The National Toxicology Program and the International Agency for Research on Cancer have labeled vinyl chloride as a definite human carcinogen.

Tobacco

To date, most studies have found no increased risk of breast cancer from active tobacco smoking. Beginning in the mid-1990s, studies have shown an increased risk of breast cancer in active smokers and those exposed to cigarette smoke compared with women who reported no exposure to tobacco smoke. In 2005, enough evidence has been gathered for the [California Environmental Protection Agency] to conclude that secondhand smoke from secondhand smokers causes breast cancer in younger women, especially premenopausal. The agency concluded that the risk was increased by 70%, based on epidemiological studies and the fact that there are many carcinogens of mammas in passive smokers. The following year (2006) the US Surgeon General identified the same increased risk and concluded that the evidence was "suggestive," one step below causal. There is some evidence that most cigarette smoke exposure is problematic between puberty and the first birth. The reason is that breast tissue looks most sensitive to chemical carcinogens, breast cells are not fully differentiated to lactation. A possible reason that the longer active smoking study did not detect the risks associated with smoking was that they compared active smokers with all smokers (which includes many passive smokers). More recent studies, which exclude passive smokers from the control group, generally indicate a high risk associated with both active and passive smoking.

Passive smoking

Passive smoker smoke increases the risk of breast cancer by up to 70% in younger women, especially pre-menopausal women. The California Environmental Protection Agency has concluded that passive smoking causes breast cancer and the US Surgeon General has concluded that the evidence was "suggestive," one step below causal. There is some evidence that most cigarette smoke exposure is problematic between puberty and the first birth. The reason why breast tissue appears most sensitive to chemical carcinogens in this phase is that breast cells are not fully differentiated to lactation.

Radiation

Women who have received high doses of ionizing radiation to the chest (for example, as a treatment for other cancers) have a relative risk of breast cancer between 2.1 and 4.0. The risk increases with increasing doses. In addition, the risk is higher in women who are irradiated before age 30, when breast development is still present.

Dioxin

Dioxins (especially dibenzodioxins polychlorinated) are chemicals produced when chlorinated products are burned, such as polyvinyl chloride (PVC). This occurs when chlorinated products are used in a particular manufacturing industry. Dioxins are also added to the air when gasoline and diesel fuel break down. Dioxins are able to accumulate bio, which means that they stay and stay in human and animal fats for long periods of time. There are many types of dioxins and only some of them are labeled by the Environmental Protection Agency as human carcinogens and endocrine disruptors. Although dioxins are floating in the air, they eventually settle on plants and other vegetation surfaces. These plants and plants are they eaten by cows and other animals. Humans end up eating the produce, milk, eggs, and meat produced by these animals that have consumed closed vegetation dioxins. Dioxins are more dangerous when ingested in this way. Several studies have led to the idea that elevated dioxin levels may increase a person's risk for breast cancer. A study conducted in 1976 after the explosion of a chemical plant in Seveso, Italy concluded that exposure to high levels of dioxin in the female body correlated with more than twice the chance of developing breast cancer.

Light at night and circadian rhythm disturbance

In 1978 Cohen et al. proposed that reducing the production of the hormone melatonin may increase the risk of breast cancer and cite "environmental lighting" as a possible contributing factor. Researchers at the National Cancer Institute (NCI) and the National Institute of Environmental Health Sciences conducted a study in 2005 showing that artificial light at night can be a factor for breast cancer by disrupting melatonin levels. According to a 2008 study, the decrease in melatonin levels in postmenopausal women was associated with a higher risk of breast cancer.

In 2007, "shift work involving circadian disorders" was listed as a possible carcinogen by the International Agency for International Cancer Research of the World Health Organization. (IARC Press release No. 180). Several studies have documented the association between night shift work and an increased incidence of breast cancer. A recent knowledge of the health consequences of artificial light exposure at night including an increased incidence of breast cancer and an explanation of causal mechanisms have been published in the Journal of Pineal Research in 2007.


Racial and socioeconomic factors

Incidents and deaths vary with race and social status. Incidence is rising with an improving economic situation, while mortality is associated with low economic status. In the US incidence was significantly lower and mortality was higher among black women and this difference seemed to persist even after adjustment for economic status. It is not currently clear whether significant racial differences in incidence and mortality persist after adjustment of economic status between white, Hispanic and Asian women in the US.

Several studies have found that black women in the US are more likely to die from breast cancer although white women are more likely to be diagnosed with the disease. Even after diagnosis, black women are less likely to get treatment than white women. Scholars have developed several theories for differences, including insufficient access to screening, reduced availability of the most advanced surgical and medical techniques, or some of the biological characteristics of the disease in African American populations. Several studies have shown that racial differences in breast cancer outcomes can reflect a cultural bias more than biological diseases. However, the lack of diversity in clinical trials for breast cancer treatment can contribute to this difference, with recent research showing that black women are more likely to have estrogen receptor negative breast cancer, which is unresponsive to effective hormone treatments for most whites. woman. Research is currently underway to determine the contribution of both biological and cultural factors.

Part of the difference in events caused by race and economic status can be explained by the use of hormone replacement therapy in the past


Factors with inconclusive research

Tea

One study published in 2009 showed that moderate green tea or black tea consumption (three or more cups per day) could reduce the risk of breast cancer by 37% in women younger than 50 years, compared with women who did not drink tea at all. But no relationship is found for women as a whole. But the study has been criticized for its inaccuracies and other studies have found no significant association between breast cancer and overall tea consumption, but found a weak inverse association between caffeine-containing drinks and the risk of post-menopausal breast cancer.

In particular about green tea, one study has found a significant inverse association between breast cancer risk and green tea intake in Asian women who are low soy consumers.

1,3-Butadiene

1,3-Butadiene is an environmental factor that can be found in air pollution and can be produced by combustion engines, as well as petroleum refineries. It is found in cigarette smoke and is also used in the manufacture and processing of certain synthetic rubber products and fungicides. The National Toxicology Program has labeled 1.3-Butadiene as a definite human carcinogen. The EPA has stated that people are primarily in contact with these chemicals through simple inhalation means.

Mammography density

Mammography density refers to the relative proportions of the radiodency area compared to the radiolucent area of ​​the mammogram, which is essentially a breast x-ray. The radiodens area of ​​the mammogram is white and associated with ductal and lobular epithelium, connective tissue and fluid in the breast. The radiolucency area is dark gray or black and is associated with fat in the breast. The high density of mammography is associated with a higher risk of developing breast cancer, but the reasons for this link are uncertain and are being studied. In contrast, patients with very low mammography breast densities were found to have a worse prognosis regardless of age, BMI and menopausal status.

Red No. 3

Red No. 3 is a dye used on some foods. In laboratory tests the DNA of human breast cells was found to be positive for damage when put into contact with Red No. 3, which means that it is genotoxic.

Virus

Several types of viruses with oncogenic potential allegedly play a role or cause breast cancer. Among the three most commonly studied are human papilloma virus (HPV), rat mammalian tumor virus (MMTV) and Epstein-Barr virus (EBV). A study published in 2011, reviewing 85 original molecular research investigations into the presence of one or more of these three viruses found that only seven studies have conclusively demonstrated the presence of oncogenic virus biomarkers, while twenty-five studies were able to show no viruses studied, and the remaining studies were excluded due to deficiencies. Thus, data from this investigation do not justify the conclusion whether HPV, MMTV, or EBV play a causal role in the development of human breast cancer.

Humans are not the only mammals that are susceptible to breast cancer. Some mice strains, ie house mice (Mus domesticus) are susceptible to breast cancer caused by mammalian rat tumor virus infection (MMTV or "Bittner virus" for its discoverer, John Joseph Bittner), with random insersional mutagenesis. This is the only animal breast cancer with a known aetiology. These findings are taken to mean that the origin of human breast cancer virus is at least possible, although there is no definitive evidence to support the claim that MMTV causes human breast cancer. For example, there may be important differences between the pathogenesis of cancer in mice and humans. The human homolog of the mammary virus has been described in 1971 and is associated with human breast cancer in several small epidemiological studies.


Factors with minimal or no impact

Abortion

The abortion-breast cancer hypothesis (ABC) suggests an induced abortion increases the risk of developing breast cancer; it is a controversial subject and the current scientific consensus has concluded that there is no significant relationship between abortion in the first trimester and the risk of breast cancer.

Bra

There is no scientific evidence to prove that any type of Brassiere can cause cancer.

Deodorant

The myth that breast cancer is associated with the use of deodorants has been widely circulated, and appears to have come from spam emails sent in 1999. But there is no evidence to support such links.

Fertility treatments

There is no persuasive relationship between fertility drugs and breast cancer.

Folic acid (folate)

The results of studies on the effect of dietary folic acid on breast cancer have been contradictory.


History

In the past centuries, the development of breast cancer is most often seen as a divine punishment or trial. From ancient Greek medicine to the late seventeenth century, the dominant medical explanation was the imbalance of the four humors. At the beginning of the 18th century, humoralism was generally rejected. Many other theories put forward, often associated with sexual activity: In 1713, Bernardino Ramazzini said that the sisters developed breast cancer at a higher rate than married women because they did not have sexual intercourse, and lack of "unnatural" sexual activity due to breast instability; others reply that the cause is too often sexual activity. Other theories of the 18th century encompassed various problems with the movement of body fluids, such as lymphatic blockage, thickened milk or remaining pus transformation after infection.

In modern times, women are more likely to blame themselves, perhaps deciding that a diet, a history of infertility, a decision not to breastfeed, or a level of exercise is the cause.


See also

  • Carcinogen # IARC classification of carcinogens
  • Epidemiology of breast cancer
  • Silent Spring Institute
  • Xenoestrogen
  • Your Disease Risk
  • Metastatic mouse breast cancer model
  • Gynecologic cancer disparities in the United States



References




External links

  • Breast cancer in Curlie (based on DMOZ)
  • GeneReviews/NCBI/NIH/UW entries on BRCA1 and BRCA2 Hereditary Breast/Ovarian Cancer
  • Breast cancer database at Silent Spring Institute
  • Risk factors for breast cancer in Curlie (based on DMOZ)

Source of the article : Wikipedia

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