Link between Early Life and Breast Anomalies

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1		Alkis Matsas	--	2728	2023-04-04 20:08:36	\|
2	format change	Peter Tang	Meta information modification	2728	2023-04-06 04:43:47	\|

This entry is adapted from the peer-reviewed paper 10.3390/children10030601

Several factors during childhood and adolescence are thought to be associated with the development of proliferative benign breast diseases and breast cancer in adulthood.

breast risk factors anomalies pathology childhood adolescence

1. Introduction

Numerous studies have tried to explore the relationship between early life exposures and the risk for benign breast disease (BBD). Relevant literature has shown that proliferative BBD may also increase the subsequent risk for breast cancer ^[1]. Understanding the influence of these factors and life events during childhood and adolescence on the development of BBD can provide information regarding the pathophysiology of breast cancer and help develop prevention strategies ^[2].

Some of the earliest epidemiological studies highlighted the role of factors such as age at menarche onset, age at first birth, total body fat, and adolescent body mass index (BMI) in determining subsequent risk of breast cancer ^[3]. These observations suggested that breast tissue may be vulnerable during the time between the onset of menarche, when the breast cells begin to proliferate, and the completion of the first pregnancy, when breast tissue undergoes terminal differentiation into milk-producing cells ^[1].

2. Dietary Factors

In 1988 deWaad and Trichopoulos proposed that an energy-rich diet during puberty and adolescence stimulates the growth of mammary glands and leads to an increased occurrence of precancerous breast lesions ^[4]. Furthermore, diet alters the hormonal environment of the breast ^[5].

In a cohort study during adolescence, Baer et al. examined the relation between type of fat and BBD. Those who were in the top quintile of animal fat consumption had a 33% increased risk of proliferative breast diseases (P-BBD), whereas women who were in the highest quintile of vegetable fat consumption had a 27% reduced risk of P-BBD. The highest quintile of monounsaturated fat consumption was associated with a relative risk of 1.52. No association with total fat consumption was found ^[6].

As far as meat consumption is concerned, several hypotheses explain how intake of red meat could induce carcinogenesis: its highly bioavailable iron content, growth- promoting hormones, carcinogenic heterocyclic amines formed in cooking, and fatty acids contained in the meat ^[7].

In a prospective cohort study of 9031 females by Berkey et al., it was found that biopsy-confirmed BBD can be associated with certain adolescent dietary factors. In particular, the authors suggested that the consumption of animal (nondairy) fat at 10 years of age was associated with a higher risk for BBD, while the consumption of nuts and peanut butter at 14 years of age was associated with a lower risk for the development of the disease. Both are individually important milestones as they represent dietary exposures before and after adolescent height growth, which is typically completed by 14 years of age ^[8].

3. Lifestyle Factors

3.1. Alcohol

According to the International Agency for Research on Cancer, alcohol is closely linked with invasive breast carcinoma ^[9]. Relatively few studies have examined the effect of alcohol consumption among young people and adolescents regarding the risk of breast cancer ^[10]^[11].

The aforementioned conclusions, along with reports suggesting that adult alcohol intake does not elevate the BBD likelihood ^[12], indicate that early life alcohol intake has the greatest effect on these breast conditions. The effect of alcohol in adolescence and risk of BBD may be particularly strong for young females with a breast cancer family history or a maternal history of BBD ^[13].

Several mechanisms have been proposed for alcohol’s effects on the breast, but it is still unknown which are responsible for increased risk of BBD and breast cancer. Proposed mechanisms include an effect on circulating hormone levels, the production of carcinogens such as acetaldehyde, and oxidative stress ^[14].

3.2. Physical Activity (PA)

Monninkof et al. found an inverse relationship between PA in adolescence and breast cancer in approximatelyhalf of the studies that assessed PA before the age of 20 ^[15]. Some studies have reported that recent PA has a stronger protective effect in comparison to PA of the distant past ^[16].

The positive impact of adolescent PA on breast malignancies prior or following menopause has been previously reported. PA, however, may need to be sustained until adulthood to retain its protective effect. In the Nurse’s Health Study II, for example, a reduced risk of premenopausal breast cancer was most apparent among women who engaged in high levels of activity during both youth (ages 12–22) and adulthood compared with women with low levels of activity during both age periods, as active women had a 30% reduction of breast cancer risk (RR = 0.70, 95% CL: 0.53–0.93) ^[17].

4. Anthropometric Factors

4.1. Body Mass Index and Weight

According to Van den Brandt et al., there is a negative correlation between adult adiposity and premenopausal breast cancer and a positive correlation between adult adiposity and postmenopausal breast cancer ^[18]. In prospective studies, childhood and adolescent adiposity show a negative correlation with breast cancer during the postmenopausal years, even after controlling for adult attained weight or BMI ^[3]. Systematic reviews and meta-analyses show an inverse trend between late adolescent BMI and premenopausal breast cancer observed in Caucasian and African heritages, though evidence from Asia is more variable ^[19].

This inverse relation to premenopausal breast cancer, described above, is also observed for proliferative BBD. Berkey et al. found that higher BMI, as measured during adolescence, was associated with slightly decreased BBD risk. Girls with a BMI in the upper two quintiles of BMI had less than half the risk (OR: 46 95% CL: 26–81) compared with those with a BMI in the lower three quintiles ^[20]. This finding was consistent with results from the NHS II, supporting that body fat composition measured in children between 5 and 10 was inversely related to P-BBD risk. This protective effect was also apparent in later adolescence: a BMI> or equivalent to 25 at age 18 was associated with a 33% reduction in BBD risk ^[21].

4.2. Growth Velocity and Height

Several studies suggest that a rapid height growth during puberty may constitute a factor for the development of cancer. When childhood growth is rapid, there is less time available for the repairment of DNA damage caused by exposures to carcinogenic factors ^[22].

A Danish study by Allgren et al., in which the annual height and weight of children was collected from school health records, reported that height growth from age 8 to 14 years was significantly associated with a high risk of developing breast cancer (RR: 1.17/5 cm increase), (CI 95%: 1.09–1.25), while growth during the peak year showed a marginally significant correlation (OR: 1.15/5 cm increase, CI: 0.97–1.36) ^[23]. In a British cohort study, it was found that rapid height growth from age 4 to 7 years, and from age 11 to 15 years, were associated with increased risk for breast cancer ^[24].

Equally interesting, in 2020, the Sisters Study Cohort, a prospective cohort study of US women with a family history of breast cancer, examined all pubertal markers in the context of their family history. It a study by Goldberg et al., it was found that women who reached their adult height at 18 years of age or later had a 13% decreased risk of developing breast cancer compared to those reaching adult height at 15–17 years of age ^[25].

5. Age at Menarche

Earlier age at menarche is related to an increased risk of premenopausal and postmenopausal breast cancer. In a meta-analysis including more than 100 epidemiological studies, each one-year decrease in age at menarche increased the risk of breast cancer by 5% ^[26]. The underlying mechanisms are not well understood but may involve higher levels of estrogen both earlier ^[27] and later ^[28] in life in girls with earlier menarche.

In the Multiethnic Cohort Study, age at menarche was associated with positive estrogen receptor (ER+) and positive progesterone receptor (PR+) breast cancer, but not with ER−/PR− breast cancer ^[29]. In addition to any hormone-mediated effects, another potential mechanism by which early age at menarche could increase breast cancer risk is the lengthening of the interval between menarche and first birth ^[30].

Furthermore, in the Sister Study, the established risk factor of earlier age at menarche was confirmed and associated with an increased risk of breast cancer for <12 years compared to 12–13 years ^[25].

The relationship between age at menarche and risk of BBD is not yet well established ^[20]. In the GUTS cohort, Berkey et al. reported an absence of correlation between age of menarche and BBD risk ^[13]^[20]. Lack of correlation between the aforementioned variables was further confirmed by several other studies ^[31].

Age at menarche is determined partially by hereditary factors, but body size, nutrition, and physical activity may also play a role ^[32]. Menarche tends to be earlier in girls with increased body fat and later in girls who exercise ^[33]. A childhood diet that is high in animal protein and low in vegetable protein may also be linked with earlier menarche ^[34].

6. Age at Thelarche

In the Sister Study cohort, Goldberg et al. thoroughly examined the age of menarche, as well as other pubertal factors in relation to breast cancer. In particular, the age of thelarche was shown to be biologically more relevant to breast cancer risk than the timing of menarche, as it represents the onset of the vulnerable period of rapid breast cell proliferation. Thelarche prior to 10 years of age was associated with a 23% greater risk of breast cancer compared with the mean age of thelarche at 12–13 years. A 3% decrease in breast cancer risk was associated with each 1-year delay in age at thelarche. The timing of thelarche was inversely associated with the risk of development both ER+ and ER− cancers ^[25].

The early onset of puberty appears to trigger the prolonged exposure of breast cells to a highly proliferative, undifferentiated state, making them more susceptible to carcinogenesis. Earlier puberty, caused by the re-activation of the hypothalamic-pituitary-gonadal axis, triggers the increase in endogenous hormones such as estrogen and insulin-like growth factor-1 (IGF-1), which regulate breast development ^[25].

7. Ionizing Radiation

Children who received therapy with chest radiation for other pediatric malignancies are known to be at increased risk of developing breast cancer later in life. Radiation exposure for girls during peak breast development, typically from 10 to 16 years of age, is associated with the highest risk. Approximately 40% of girls treated with radiation for Hodgkin lymphoma will develop breast cancer; it takes an average of 20 years for it to appear ^[35].

Breast cancer risk is greatest among women treated for Hodgkin’s lymphoma with high-dose mantle radiation, but it is also elevated among women who received moderate-dose chest radiation (e.g., mediastinal, lung) for other pediatric and young adult cancers, such as non-Hodgkin’s lymphoma, Wilms tumor, leukemia, bone cancer, neuroblastoma, and soft tissue sarcoma ^[36].

Inskip et al. reported that the risk of being diagnosed with breast cancer increased with chest radiation dose, reaching 10.8 (95% CI: 3.8–31) for 40 Gy compared to those who received no radiation ^[37]. In addition, a later study found that among women treated for childhood cancer with chest radiation therapy, those treated with whole-lung irradiation have a greater risk of breast cancer, demonstrating the importance of radiation volume ^[38].

Evidence has also suggested that the risk could be associated with radiation field volume, due to the increased risk (odds ratio 2.7 (95% CI, 1.1–6.9) of women treated with mantle field irradiation compared to women with similarly dosed mediastinal irradiation (omitting the axillary nodes) ^[39].

In a study by Schellong et al., up to July 2012, secondary breast cancer was diagnosed in 26 of 590 female patients with Hodgkin disease (HD). Their age at time of treatment for HD was 9.9 to 16.2 years. Radiation to the supradiaphragmatic fields was between 20 and Gy. The cumulative incidence for secondary breast disease 30 years after treatment for HD was 19% (95% CI, 12% to 29%). Women aged 25 to 45 reported a frequency of breast cancer 24 times as high as in the corresponding normal population ^[40].

Given that radiation therapy is a confirmed risk factor for a second breast cancer, Charlotte Demoor-Goldschmidt et al. characterized for the first time the histological subtypes and the hormonal receptor status of radiation therapy-induced SBC among survivors of a childhood or young adult cancer. In particular, a multicenter retrospective study of 121 women was conducted, with the mean age of the first cancer diagnosis at 15 years and at initial SBC diagnosis at 38 years of age. The main finding of the study associated radiation doses greater than 20 Gy to the mediastinum with triple negative phenotype breast cancers, which in turn were related to an aggressive histoprognostic status ^[41].

8. Anthracyclines

In 2016, Henderson et al. attempted to identify the risk factors for breast cancer among childhood cancer survivors who did not receive chest radiotherapy. Henderson et al. conducted the Childhood Cancer Survivor Study, in which 3768 females without a history of chest radio therapy as part of their cancer treatment plan during childhood participated. The development of subsequent breast cancer, on the ground of nonirradiated field, was associated with exposure to anthracyclines or alkylators. Henderson et al. reported a 2.5- to 6-fold increased risk of breast cancer in women received anthracycline chemotherapies. The findings of the study confirmed the potential of anthracycline agents to trigger malignant transformations in mammalian cell systems as well as the ability of alkylators to disrupt cancer growth or cause DNA damage ^[42].

Following the previous study, in 2019Ehrhardt et al. tried to clarify the relation between anthracycline-associated risk for the development of subsequent breast cancer and TP-53 mutation-related gene-environment interactions. In the context of this cohort study, in which the participants were 1467 childhood cancer survivors who were treated at St Jude Children’s Research Hospital, a greater than 13-fold risk for breast cancer in women who received 250 mg/m² or more of anthracycline was observed. Furthermore, breast cancer predisposition gene mutations were identified, and it was suggested that the anthracycline treatment-related risk was independent of autosomal dominantly inherited cancer predisposition mutations, especially for TP53 ^[43].

9. Socioeconomic Status

In 2017, Hiatt et al. described the impact of socioeconomic position (SEP) on pubertal onset. In more detail, puberty onset was assessed based on the standard methods of Tanner staging and defined by observation and palpation of breast budding for stages B2 or higher as well as by observation of stages PH2 and higher.

The main finding of this prospective cohort study was that girls in the lowest SEP index quantile tend to develop pubertal signs of breast budding 7 months earlier than girls in the highest SEP quantile. Given that earlier onset of female reproductive maturity is associated with increased breast cancer rates in adulthood, SEP could be indirectly related to breast pathologies. SEP, therefore, may influence breast and generally pubertal development onset ^[44].

10. Smoking and Drug Abuse

With regard to BBD, there is limited data available. Cui et al. reported no increased risk of postmenopausal, benign proliferative epithelial disorder (BPED) among women who started smoking during adolescence ^[45]. Regarding breast cancer risk, a review by Okasha et al. published in 2003 concluded that the data supporting an association between smoking at a young age and breast cancer risk is inconsistent, and the same applied for passive smoking in early life, highlighting the need for further studies to evaluate this relationship ^[46]. However, a more recent study showed the opposite; a study by Jones et al. concluded that smoking was associated with an increased risk of breast cancer, particularly in women who began smoking during adolescence as well as in women with a family history of the disease ^[47]. Interestingly enough, a study by Liu et al. demonstrated that exposure to heavy cigarette smoking during the prenatal period could be associated with an increased risk of BBD in adulthood ^[48].

11. Other Factors

Limited data have suggested an association between drug and antibiotic abuse during late adolescence and breast cancer. A study by Dahlman et al., including 3,838,248 women aged 15–75 years in Sweden, concluded that women with drug use disorders constitute a risk group for incident, fatal, and metastasized breast cancer ^[49].Furthermore, a study by Velicer et al., including patients who were at least 19 years old, showed that cumulative days of antibiotic use, especially as a treatment for respiratory tract infections, constitutes a risk factor for the development of breast cancer ^[50]. However, both studies could not determine if the medication use was causally related to breast cancer. This has also been confirmed by a recently published meta-analysis by Simin et al., highlighting the need for further studies to examine this relationship ^[51].Evidence has also highlighted the anticancer properties of Vitamin D in relation to breast cancer ^[52]. Researchers hypothesize that this could explain the seasonality of the diagnosis, with the highest diagnosis rates during spring and autumn, as solar ultraviolet radiation B through the production of vitamin D lowers the risk for the disease in summer and higher concentrations of melatonin reduce the risk during winter ^[53]. Interestingly, serum 25(OH)D concentrations have also been associated with the risk for breast cancer; the risk increased rapidly as serum concentrations decreased below 12 ng/mL ^[52]. Lastly, Vitamin D from sunlight exposure has been associated with a lower risk of fatal breast cancer ^[54].

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Panagiotis Christopoulos

Alkis Matsas

Makarios Eleftheriades

Georgia Kotsira

Anna Eleftheriades

Nikolaos F. Vlahos

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Update Date: 06 Apr 2023

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