Reproductive Factors in Breast Cancer Epidemiology

Kvåle, Gunnar

doi:10.3109/02841869209088901

Cited by 57 publications

(24 citation statements)

References 84 publications

(60 reference statements)

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“…Early age of menarche is associated with breast cancer and cardiovascular disease (Kvale 1992; Lakshman, et al 2009). Therefore it is important to understand the mechanisms controlling puberty initiation.…”

Section: Resultsmentioning

confidence: 99%

A new pathway in the control of the initiation of puberty: the MKRN3 gene

Abreu¹,

Macedo²,

Brito³

et al. 2015

Journal of Molecular Endocrinology

111

104

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Pubertal timing is influenced by complex interactions among genetic, nutritional, environmental, and socioeconomic factors. The role of MKRN3, an imprinted gene located in the Prader-Willi syndrome critical region (chromosome 15q11-q13), in pubertal initiation was first described in 2013 after the identification of deleterious MKRN3 mutations in five families with central precocious puberty (CPP) using whole-exome sequencing analysis. Since then, additional loss-of-function mutations of MKRN3 have been associated with the inherited premature sexual development phenotype in girls and boys from different ethnic groups. In all of these families, segregation analysis clearly demonstrated autosomal dominant inheritance with complete penetrance, but with exclusive paternal transmission, consistent with the monoallelic expression of MKRN3 (a maternally imprinted gene). Interestingly, the hypothalamic Mkrn3 mRNA expression pattern in mice correlated with a putative inhibitory input on puberty initiation. Indeed, the initiation of puberty depends on a decrease in factors that inhibit the release of GnRH combined with an increase in stimulatory factors. These recent human and animal findings suggest that MKRN3 has an inhibitory role in the reproductive axis to represent a new pathway in pubertal regulation.

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Section: Resultsmentioning

confidence: 99%

A new pathway in the control of the initiation of puberty: the MKRN3 gene

Abreu¹,

Macedo²,

Brito³

et al. 2015

Journal of Molecular Endocrinology

111

104

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“…The same is true for the recent breast cancer review 7 published in The Lancet. Reviewers who have included a discussion of induced abortion as a real or potential risk factor have not been comprehensive, [8][9][10][11][12] and also often fail (as do many ofthe original epidemiological studies) to distinguish between induced and spontaneous abortion.89 Even when the distinction is made, erroneous citations are common. For example, Table 1 Epidemiological studies on abortion and breast cancer incidence which do not report specific data on induced abortion Author(s) Year Nation of study population Overall OR (everlnever) Significant?…”

mentioning

confidence: 99%

Induced abortion as an independent risk factor for breast cancer: a comprehensive review and meta-analysis.

Brind

Chinchilli²,

Severs

et al. 1996

Journal of Epidemiology & Community Health

109

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Study objective -To ascertain, from the published reports to date, whether or not a significantly increased risk ofbreast cancer is specifically attributable to a history of induced abortion, independent of spontaneous abortion and age at first full term pregnancy (or first live birth); to establish the relative magnitude of such risk increase as may be found, and to ascertain and quantify such risk increases as may pertain to particular subpopulations of women exposed to induced abortion; in particular, nulliparous women and parous women exposed before compared with after the first full term pregnancy. Included studies -The meta-analysis includes all 28 published reports which include specific data on induced abortion and breast cancer incidence. Since some study data are presented in more than one report, the 28 reports were determined to constitute 23 independent studies. Overall induced abortion odds ratios and odds ratios for the different subpopulations were calculated using an average weighted according to the inverse of the variance. An overall unweighted average was also computed for comparison. No quality criteria were imposed, but a narrative review of all included studies is presented for the reader's use in assessing the quality of individual studies. Excluded studies -All 33 published reports including data on abortion and breast cancer incidence but either pertaining only to spontaneous abortion or to abortion without specification as to whether it was induced or spontaneous. These studies are listed for the reader's information. Results -The overall odds ratio (for any induced abortion exposure; n = 21 studies) was 1.3 (95% confidence interval of 1.2, 1.4). For comparison, the unweighted overall odds ratio was 1.4 (1.3,1.6). The odds ratio for nulliparous women was 1.3 (1.0,1.6), that for abortion before the first term pregnancy in parous women was 1.5 (1.2,1.8), and that for abortion after the first term pregnancy was 1.3 (1.1,1.5).Conclusions -The results support the inclusion of induced abortion among significant independent risk factors for breast cancer, regardless of parity or timing of abortion relative to the first term pregnancy. Although the increase in risk was relatively low, the high incidence of both breast cancer and induced abortion suggest a substantial impact of thousands of excess cases per year currendy, and a potentially much greater impact in the next century, as the first cohort of women exposed to legal induced abortion continues to age.

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“…Genetic variation affecting events associated with puberty may relate to future disease risks. For example, previous studies have linked younger menarcheal age to increased later-in-life risks of obesity, type 2 diabetes, breast and endometrial cancer, and cardiovascular diseases[2–5]. During puberty, timing of menarche is in general well synchronized with somatic change.…”

Section: Introductionmentioning

confidence: 99%

Associations Between Menarche-Related Genetic Variants and Pubertal Growth in Male and Female Adolescents

Wagner

Eckert

et al. 2015

Journal of Adolescent Health

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Purpose Previous studies have identified novel genetic variants associated with age at menarche in females of European descent. The pubertal growth effects of these variants have not been carefully evaluated in non-European descent groups. We aimed to examine the effects of 31 newly identified menarche-related single nucleotide polymorphisms (SNPs) on growth outcomes in African American (AA) and European American (EA) children in a prospective cohort. Methods We analyzed longitudinal data collected from 263 AA and 338 EA enrolled between ages 5 and 17 years; the subjects were followed semiannually for an average of 6 years. The associations between the SNPs and growth-related outcomes, including weight, height, and body mass index (BMI), were examined using mixed-effect models. Results Longitudinal analyses revealed that 4 (near or in genes VGLL3, PEX2, CA10, and SKOR2) out of the 14 menarche-only related SNPs were associated with changes in weight and BMI in EA and AA (P≤0.0032), but none of them were associated with changes in height. Of the 8 menarche-timing and BMI-related SNPs, none was associated with changes in height, but 3 (in or near genes NEGR1, ETV5, and FTO) were associated with more rapid increases in weight and/or BMI in EA (P≤0.0059). Among the 9 menarche-timing and height-related SNPs, 4 (in or near genes ZBTB38, LOC728666, TBX2 and CABLES) were associated with changes in weight or height in EA and AA (P≤0.0042). Conclusion Genetic variants related to age at menarche were found to be associated with various growth parameters in healthy adolescents. The identified associations were often race and sex-specific.

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Reproductive Factors in Breast Cancer Epidemiology

Cited by 57 publications

References 84 publications

A new pathway in the control of the initiation of puberty: the MKRN3 gene

A new pathway in the control of the initiation of puberty: the MKRN3 gene

Induced abortion as an independent risk factor for breast cancer: a comprehensive review and meta-analysis.

Associations Between Menarche-Related Genetic Variants and Pubertal Growth in Male and Female Adolescents

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