Risk factors for breast cancer
If a mother or a sister was diagnosed breast cancer, the risk of a hereditary BRCA1 or BRCA2 gene mutation is about two-fold higher than those women without a familial history.
[11] Hereditary non-BRCA1 and non-BRCA2 breast tumors (and even some sporadic carcinomas) are believed to result from the expression of weakly penetrant but highly prevalent mutations in various genes.
For instance, polymorphism has been identified in genes associated to the metabolism of estrogens and/or carcinogens (Cytochrome P450, family 1, member A1, CYP1B1, CYP17A1, CYP19, Catechol-O-methyltransferase, N-acetyltransferase 2, Glutathione S-transferase Mu 1, GSTP1, GSTT, .
[37] Furthermore, studies have shown that obese women are more likely to have large tumors, greater lymph node involvement, and poorer breast cancer prognosis with 30% higher risk of mortality.
[39] However, other cohort studies and recent clinical trials have not shown a significant relationship between weight gain after diagnosis and breast cancer mortality.
Seventeen scientific studies in the United States have found that as obesity increases in women over 40 years of age the rate of mammography reported decreases significantly.
[45] Other reasons obese women may avoid mammography are due to lack of insurance, low income, or embarrassment at the procedure, although when these factors are accounted for, the effect of lower rates of screening are still significant.
Hormonal contraceptives may produce a slight increase in the risk of breast cancer diagnosis among current and recent users, but this appears to be a short-term effect.
Further, the cancers diagnosed in women who had ever used hormonal contraceptives were less advanced than those in nonusers, raising the possibility that the small excess among users was due to increased detection.
The largest meta-analysis (1997) of data from 51 observational studies, indicated a relative risk of breast cancer of 1.35 for women who had used HRT for five or more years after menopause.
One of the adverse outcomes prompting closure was a significant increase in both total and invasive breast cancers (hazard ratio = 1.24) in women randomized to receive estrogen and progestin for an average of five years.
[76] According to a review, the main mechanisms by which environmental compounds increase breast cancer risk are acting like hormones, especially estrogen, or affecting susceptibility to carcinogenesis.
[77] The evidence to date generally supports an association between breast cancer and polycyclic aromatic hydrocarbons (PAHs) and polychlorinated biphenyls (PCBs).
At very low levels the FDA has long considered BPA in food to be safe, but this has been challenged over the years as more information is discovered regarding the effects of the chemical.
Animals exposed to BPA during fetal life develop palpable tumors, and all studies show an increased susceptibility to mammary gland neoplasia that manifests during adulthood.
It was concluded that perinatal exposure to low doses of BPA results in altered mammary gland morphogenesis, induction of precancerous lesions, and carcinoma in situ.
Studies have shown that women who eat higher amounts of overcooked meat, meaning more exposure to heterocyclic amines, have also been diagnosed with more post-menopausal breast cancer.
Heterocyclic amines also have the ability to copy estrogen and in laboratory studies have been found to encourage the growth of cancerous tumors on human tissue.
[85] Although the pesticide DDT was banned in the United States in the 1970s,[86] studies have shown that there are still trace amounts found in certain agricultural products, as well as in human and animal milk.
[87] While individual studies have come to conflicting conclusions, the most recent reviews of all the evidence conclude that exposure to DDT before puberty increases the risk of breast cancer later in life.
A study done by the US 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 medical sterilization processes.
[90] By 2005 enough evidence had accumulated for the California Environmental Protection Agency to conclude that breathing secondhand smoke causes breast cancer in younger, primarily premenopausal women.
A study done in 1976 after a chemical plant explosion in Seveso, Italy, concluded that high dioxin level exposure in a woman's body correlated with a more than double chance of developing breast cancer.
[85] In 1978 Cohen et al. proposed that reduced production of the hormone melatonin might increase the risk of breast cancer and citing "environmental lighting" as a possible causal factor.
[97] In 2007, "shiftwork that involves circadian disruption" was listed as a probable carcinogen by the World Health Organization's International Agency for Research on Cancer.
[99][100][101][102] A review of current knowledge of the health consequences of exposure to artificial light at night including the increased incidence of breast cancer and an explanation of the causal mechanisms has been published in the Journal of Pineal Research in 2007.
It is currently unclear if significant ethnic differences in incidence and mortality persist after adjustment for economic status between women of white, Hispanic and Asian origin in the US.
[114][115] Conversely, patients with very low mammographic breast density were found to hold a poorer prognosis irrespective of age, BMI and menopausal status.
Thus, the data from these investigations do not justify a conclusion as to whether HPV, MMTV, or EBV play a causal role in human breast cancer development.
[132] Other theories from the 18th century included various sorts of problems with the movement of body fluids, such as lymphatic blockages, curdled breast milk or the transformation of pus left after an infection.
