Abstract
Perinatal events and conditions, notably birth weight, are associated with breast cancer risk in offspring, and correlates of mammary gland mass are predictors of breast cancer risk. These findings may be interpreted as indicating that high levels of estrogens and components of the insulin-like growth factor system during pregnancy favour the generation of mammary tissue-specific stem cells, and that the number of these cells, which is positively associated with mammary gland mass, is an important determinant of breast cancer risk. Perinatal events and conditions may also affect risk for other malignancies, but the evidence in the case of breast cancer is prominent, possibly because estrogens and the insulin-like growth factor system are both involved in breast cancer etiology and affect birth weight.
Highlights
An etiologic model should explain as many of the epidemiologic characteristics of a disease as possible, as well as the results of analytical epidemiologic studies with specific objectives
Breast cancer incidence increases with age throughout the world, but the slope of the increase decreases after the menopause
Mutations in BRCA1 and BRCA2, as well as highly In this part of the review we examine the extent to which penetrant mutations in genes such as p53, CHEK2, and the etiological model we present accommodates the PTEN/MMAC1, account for a large proportion of familial epidemiology of breast cancer
Summary
An etiologic model should explain as many of the epidemiologic characteristics of a disease as possible, as well as the results of analytical epidemiologic studies with specific objectives. It is not necessary for each hormone to have a quantitatively similar breast cancer risk implication per standard deviate, and the proposed model’s third postulate accommodates any role that may be played by differential hormone receptor expression [39,40] This postulate accommodates several breast cancer risk factors: the inflection of breast cancer incidence after menopause; the increased risk for this disease with earlier menarche and later menopause; the protective effect of a surgical menopause with oophorectomy; the transient increase in risk following a pregnancy; the increased risk among overweight postmenopausal women and the positive association with breast cancer risk of alcohol drinking (which tends to increase estrogen levels); hormone replacement therapy; and – weakly – oral contraceptives. The third postulate explains how cells at risk are removed generation of mammary tissue-specific stem cells, and the through terminal differentiation or related processes The number of these cells, which is positively associated with whole model is in agreement with the results of theoretical mammary gland mass, is an important determinant of exercises and speculations undertaken long ago by breast cancer risk.
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