Risk factors can be divided into two categories: * modifiable risk factors (things that people can change themselves, such as consumption of alcoholic beverages), and * fixed risk factors (things that cannot be changed, such as age and physiological sex). The primary risk factors for<unk>  are being female and older age. Other potential risk factors include genetics, lack of childbearing or lack of breastfeeding, higher levels of certain hormones, certain dietary patterns, and obesity. One study indicates that exposure to light pollution is a risk factor for the development of<unk> . If all adults maintained the healthiest possible lifestyles, including not drinking alcoholic beverages, maintaining a healthy body composition, never smoking, eating healthful food, and other actions, then almost a quarter of<unk>  cases worldwide could be prevented. The remaining three-quarters of<unk>  cases cannot be prevented through lifestyle changes. Lifestyle All types of alcoholic beverages, including beer, wine, or liquor, cause<unk> . Drinking alcoholic beverages increases the risk of<unk> , even among very light drinkers (women drinking less than half of one alcoholic drink per day). The risk is highest among heavy drinkers. Globally, about one in 10 cases of<unk>  is caused by women drinking alcoholic beverages. Drinking alcoholic beverages is among the most common modifiable risk factors. The correlation between obesity and<unk>  is anything but linear. Studies show that those who rapidly gain weight in adulthood are at higher risk than those who have been overweight since childhood. Likewise excess fat in the midsection seems to induce a higher risk than excess weight carried in the lower body. This implies that the food one eats is of greater importance than one's BMI. Dietary factors that may increase risk include a high-fat diet and obesity-related high cholesterol levels. Dietary iodine deficiency may also play a role. Evidence for fiber is unclear. A 2015 review found that studies trying to link fiber intake with<unk>  produced mixed results. In 2016, a tentative association between low fiber intake during adolescence and<unk>  was observed. Smoking tobacco appears to increase the risk of<unk> , with the greater the amount smoked and the earlier in life that smoking began, the higher the risk. In those who are long-term smokers, the relative risk is increased 35% to 50%. A lack of physical activity has been linked to about 10% of cases. Sitting regularly for prolonged periods is associated with higher mortality from<unk> . The risk is not negated by regular exercise, though it is lowered. Hormone therapy to treat menopause is also associated with an increased risk of<unk> . The use of hormonal birth control does not cause<unk>  for most women; if it has an effect, it is small (on the order of 0.01% per user–year; comparable to the rate of maternal mortality in the United States), temporary, and offset by the users' significantly reduced risk of ovarian and endometrial<unk> s. Among those with a family history of<unk> , use of modern oral contraceptives does not appear to affect the risk of<unk> . It is less certain whether hormonal contraceptives could increase the already high rates of<unk>  in women with mutations in the<unk>  susceptibility genes<unk> 1 or<unk> 2. Breast feeding reduces the risk of several types of<unk> s, including<unk> . In the 1980s, the abortion–breast<unk>  hypothesis posited that induced abortion increased the risk of developing<unk> . This hypothesis was the subject of extensive scientific inquiry, which concluded that neither miscarriages nor abortions are associated with a heightened risk for<unk> . Other risk factors include radiation and circadian disruptions related to shift-work and routine late-night eating. A number of chemicals have also been linked, including polychlorinated biphenyls, polycyclic aromatic hydrocarbons, and organic solvents Although the radiation from mammography is a low dose, it is estimated that yearly screening from 40 to 80 years of age will cause approximately 225 cases of fatal<unk>  per million women screened. Genetics Genetics is believed to be the primary cause of 5–10% of all cases. Women whose mother was diagnosed before 50 have an increased risk of 1.7 and those whose mother was diagnosed at age 50 or after has an increased risk of 1.4. In those with zero, one or two affected relatives, the risk of<unk>  before the age of 80 is 7.8%, 13.3%, and 21.1% with a subsequent mortality from the disease of 2.3%, 4.2%, and 7.6% respectively. In those with a first degree relative with the disease the risk of<unk>  between the age of 40 and 50 is double that of the general population. In less than 5% of cases, genetics plays a more significant role<unk> using a hereditary breast–ovarian<unk>  syndrome. This includes those who carry the<unk> 1 and<unk> 2 gene mutation. These mutations account for up to 90% of the total genetic influence with a risk of<unk>  of 60–80% in those affected. Other significant mutations include p53 (Li–Fraumeni syndrome), PTEN (Cowden syndrome), and STK11 (Peutz–Jeghers syndrome), CHEK2, ATM, BRIP1, and PALB2. In 2012, researchers said that there are four genetically distinct types of the<unk>  and that in each type, hallmark genetic changes lead to many<unk> s. Other genetic predispositions include the density of the breast tissue and hormonal levels. Women with dense breast tissue are more likely to get tumors and are less likely to be diagnosed with<unk>  – because the dense tissue makes tumors less visible on mammograms. Furthermore, women with naturally high estrogen and progesterone levels are also at higher risk for tumor development. Medical conditions Breast changes like atypical ductal hyperplasia and lobular carcinoma in situ, found in benign breast conditions such as fibrocystic breast changes, are correlated with an increased<unk>  risk. Diabetes mellitus might also increase the risk of<unk> . Autoimmune diseases such as lupus erythematosus seem also to increase the risk for the acquisition of<unk> . The major causes of sporadic<unk>  are associated with hormone levels.<unk>  is promoted by estrogen. This hormone activates the development of breast throughout puberty, menstrual cycles and pregnancy. The imbalance between estrogen and progesterone during the menstrual phages causes cell proliferation. Moreover, oxidative metabolites of estrogen can increase DNA damage and mutations. Repeated cycling and the impairment of repair process can transform a normal cell into pre-malignant and eventually malignant cell through mutation. During the premalignant stage, high proliferation of stromal cells can be activated by estrogen to support the development of<unk> . During the ligand binding activation, the<unk> n regulate gene expression by interacting with estrogen response elements within the promotor of specific genes. The expression and activation of ER due to lack of estrogen can be stimulated by extracellular signals. Interestingly, the ER directly binding with the several proteins, including growth factor receptors, can promote the expression of genes related to cell growth and survival. Raised prolactin levels in the blood are associated with increased risk of<unk> .
Breast cancer
Mastitis
Ovarian cancer
Fibrocystic breast changes
Prostate cancer
Breast disease
Skin cancer
Cervical cancer