Cancer risk related to mammary gland structure and development

Russo, José; Yun, Hu; Silva, Ismael D.C.G.; Russo, Irma H.

doi:10.1002/1097-0029(20010115)52:2<204::aid-jemt1006>3.0.co;2-f

Cited by 131 publications

(96 citation statements)

References 99 publications

(104 reference statements)

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“…Time interval as a risk indicator in grand multiparous women A Kauppila et al predispose to breast cancer (Lagiou et al, 2003) has been supported by findings in experimental animal studies that an interaction of carcinogen with an undifferentiated breast epithelium is a prerequisite for carcinogenic initiation (Russo et al, 2001). It is possible that an insufficiently maturated breast of the young mother after her first childbirth -remains susceptible to carcinogenic effects, including hormonal influences.…”

Section: Discussionmentioning

confidence: 98%

“…Because lactation participates in the differentiation of mammary epithelium in its terminal phase (Russo and Russo, 1994b;Russo et al, 2001Russo et al, , 2008, deficient breastfeeding of the first child might leave the breast cells susceptible to carcinogenic influences. This would be in accordance with the finding that lactation has a significant independent protective effect in breast cancer (Byers et al, 1985;Collaborative Group of Hormonal Factors in Breast Cancer, 2002;Ursin et al, 2005), particularly before menopause (Byers et al, 1985;Newcomb et al, 1994;Lord et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

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Birth intervals and breast cancer risk

et al. 2009

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BACKGROUND: The interval between successive births (birth interval) may affect breast cancer risk, whereas interval from last birth to cancer onset may modify its behaviour. METHODS: The study cohort consisted of 29 488 Finnish grand multiparous (GM) women, including 628 women with breast cancer. Conditional logistic regression for case -control design nested within the cohort was used to estimate proportional hazards (referred as relative risks, RR). Age at first birth and parity were co-variables. RESULTS: Short interval (o1 year) between first and second birth increased the risk of advanced ductal breast cancer at ages o 50 years (RR ¼ 5.29; 95% CI 2.00 -14.0) as compared to interval 3 þ years. The risk of advanced ductal cancer was also large (RR ¼ 4.00; 95% CI 1.19 -13.4) shortly (o3 years) after last birth as compared with the period 15 þ years. CONCLUSIONS: Short birth interval-associated excess breast cancer risk may be related to stimulatory effects of female steroid hormones produced during two closely connected pregnancies, or defective breast maturation owing to failures in breastfeeding.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Birth intervals and breast cancer risk

et al. 2009

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“…Several cellular mechanisms have been proposed for the hormone-induced protection of breast cancer. These include a differentiation hypothesis, in which it is proposed that differentiation of the mammary gland, similar to that induced by pregnancy or hormones, results in the removal of a population of cancersusceptible cells (present in terminal end buds) and hence confers protection against breast cancer (39)(40)(41). A corollary to this hypothesis is that differences in susceptibility to carcinogeninduced tumorigenesis between parous and AMV glands could be explained by the differences in proliferation indices, alterations of the properties associated with carcinogen uptake, binding and metabolism, and an enhanced capacity for DNA repair (40)(41)(42)(43)(44).…”

Section: Discussionmentioning

confidence: 99%

p53 is a potential mediator of pregnancy and hormone-induced resistance to mammary carcinogenesis

Sivaraman

Conneely

Medina

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

117

102

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Full-term pregnancy early in reproductive life is protective against breast cancer in women. Pregnancy also provides protection in animals against carcinogen-induced breast cancer, and this protection can be mimicked by using the hormones estrogen and progesterone. The molecular mechanisms that form the basis for this protective effect have not been elucidated. On the basis of our results, we propose a cell-fate hypothesis. At a critical period in adolescence the hormonal milieu of pregnancy affects the developmental fate of a subset of mammary epithelial cells and its progeny, which results in persistent differences in molecular pathways between the epithelial cells of hormone-treated and mature virgin mammary glands. These changes in turn dictate the proliferative response to carcinogen challenge and include a block in carcinogen-induced increase in mammary epithelial cell proliferation and an increased and sustained expression of nuclear p53 in the hormone-treated mammary gland. This hormone-induced nuclear p53 is transcriptionally active as evidenced by increased expression of mdm2 and p21 (CIP1͞WAF1). Importantly, exposure to perphenazine, a compound that induces mammary gland differentiation but does not confer protection, does not induce p53 expression, indicating that p53 is not a differentiation marker. The proliferative block and induction of p53 are operative in both rats and mice, results that support the generality of the proposed hypothesis.T he lifetime risk of developing breast cancer among Western women is Ϸ10%, and despite advances in therapeutic strategies, breast cancer remains the leading cause of cancer deaths in women in most developed countries (1). Prevention of the disease can be achieved with better understanding of the etiological factors contributing to the development of the disease. There is significant evidence that the timing of normal developmental events like menarche, menopause, and age of first parity have a significant impact on an individual's susceptibility to breast cancer (2, 3). In particular, there is strong epidemiological evidence that women who experience a full-term pregnancy early in their lives have a significantly reduced risk for developing breast cancer (3-5). This is recapitulated in rat models that demonstrate that early full-term pregnancy confers resistance to chemical carcinogen-induced mammary tumorigenesis (6-11). This protection can be mimicked with the hormones estrogen (E) and progesterone (P; refs. 9 and 12) or human CG (13) given either before or immediately after carcinogen challenge to induce a refractory state.Despite a wealth of literature supporting the role of endocrinological processes in mediating parity-related refractoriness, the cellular and molecular mechanisms that underlie hormone-induced refractoriness are largely unresolved. The utility of the rodent models in which a defined hormonal regimen can be used to mimic the protective effect of pregnancy is well documented (9-17).Differing hypotheses to explain the protective effects have ...

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“…Estrogens are critical to the proliferation of breast tissue and development of the mammary gland, and early age of menarche, as well as late menopause, and late age at first birth are proxies for estrogen burden and known risk factors for breast cancer. [99][100][101] Early environmental exposures that mimic estrogens, such as bisphenol A, 102 atrazine, 103 and polyaromatic hydrocarbons, 104 may be related to earlier breast development, thereby putting the rapidly proliferating mammary tissue at risk. Chemicals that are associated with early menarche, such as polybrominated biphenyls 105 and dichlorodiphenyldichloroethylene, 106 are also of interest.…”

Section: Breast Cancermentioning

confidence: 99%

Public Health Implications of Altered Puberty Timing

et al. 2008

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Changes in puberty timing have implications for the treatment of individual children, for the risk of later adult disease, and for chemical testing and risk assessment for the population. Children with early puberty are at a risk for accelerated skeletal maturation and short adult height, early sexual debut, potential sexual abuse, and psychosocial difficulties. Altered puberty timing is also of concern for the development of reproductive tract cancers later in life. For example, an early age of menarche is a risk factor for breast cancer. A low age at male puberty is associated with an increased risk for testicular cancer according to several, but not all, epidemiologic studies. Girls and, possibly, boys who exhibit premature adrenarche are at a higher risk for developing features of metabolic syndrome, including obesity, type 2 diabetes, and cardiovascular disease later in adulthood. Altered timing of puberty also has implications for behavioral disorders. For example, an early maturation is associated with a greater incidence of conduct and behavior disorders during adolescence. Finally, altered puberty timing is considered an adverse effect in reproductive toxicity risk assessment for chemicals. Recent US legislation has mandated improved chemical testing approaches for protecting children's health and screening for endocrinedisrupting agents, which has led to changes in the US Environmental Protection Agency's risk assessment and toxicity testing guidelines to include puberty-related assessments and to the validation of pubertal male and female rat assays for endocrine screening.

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Cancer risk related to mammary gland structure and development

Cited by 131 publications

References 99 publications

Birth intervals and breast cancer risk

Birth intervals and breast cancer risk

p53 is a potential mediator of pregnancy and hormone-induced resistance to mammary carcinogenesis

Public Health Implications of Altered Puberty Timing

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