Birth characteristics and breast cancer risk: A study among like‐sexed twins

Hübinette, Anna; Lichtenstein, Paul; Ekbom, Anders; Cnattingius, Sven

doi:10.1002/1097-0215(200002)9999:9999<::aid-ijc1025>3.3.co;2-h

Cited by 48 publications

(51 citation statements)

References 13 publications

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“…Similar to several previous reports, we found a linear association between breast cancer and birth weight. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17] We also found an inverse association between birth weight and testicular cancer, which thereby strengthens the previous findings. [40][41][42][43][44][45][46] To our knowledge, only 2 smaller studies published to date have previously addressed the association between the overall risk of cancer and birth weight.…”

Section: Discussionsupporting

confidence: 88%

Birth weight and risk of cancer

Ahlgren

Wohlfahrt

Olsen

et al. 2007

Cancer

135

106

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Cones are critically dependent on interphotoreceptor retinoid‐binding protein (IRBP) for retinoid delivery in the visual cycle. Cone‐dominant vertebrates offer an opportunity to uncover the molecular basis of IRBP's role in this process. Here, we explore the association of IRBP with the interphotoreceptor matrix (IPM) of cones vs. rods in cone dominant retinas from chicken (Gallus domesticus), turkey (Meleagris gallopavo), and pig (Sus scrofa). Retinas were detached and fixed directly or washed in saline prior to fixation. Disassociated photoreceptors with adherent matrix were also prepared. Under 2 mM CaCl2, insoluble matrix was delaminated from saline washed retinas. The distribution of IRBP, as well as glycans binding peanut agglutinin (cone matrix) and wheat germ agglutinin (rod/cone matrix), was defined by confocal microscopy. Retina flat mounts showed IRBP diffusely distributed in an interconnecting, lattice‐like pattern throughout the entire matrix. Saline wash replaced this pattern with fluorescent annuli surrounding individual cone outer segments. In isolated cones and matrix sheets, IRBP colocalized with the peanut agglutinin binding matrix glycans. Our results reveal a wash‐resistant association of IRBP with a matrix domain immediately surrounding cone outer segments. The cone matrix sheath may be responsible for IRBP‐mediated cone targeting of 11‐cis retinoids. J. Comp. Neurol., 2012. © 2011 Wiley Periodicals, Inc.

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Section: Discussionsupporting

confidence: 88%

Birth weight and risk of cancer

Ahlgren

Wohlfahrt

Olsen

et al. 2007

Cancer

135

106

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“…These studies show that women who were exposed to high foetal oestrogenic environment; that is, had a high birth weight or are twins, are at an increased risk of developing breast cancer (Braun et al, 1995;Michels et al, 1996;Sanderson et al, 1996;Weiss et al, 1997). At a particularly high risk are twins whose birth weight was high (Hubinette et al, 2001). A recent study also found that women exposed to the synthetic oestrogen diethylstilbestrol (DES) in utero are at an increased risk of developing breast cancer (Palmer et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

In utero alcohol exposure increases mammary tumorigenesis in rats

et al. 2004

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Findings in humans and animal models suggest that in utero hormonal and dietary exposures increase later breast cancer risk. Since alcohol intake by adult women consistently increases their breast cancer risk, we wondered whether maternal alcohol consumption during pregnancy increases female offspring's mammary tumorigenesis. In our study, pregnant female rats were pair-fed isocaloric diets containing either 0 (control), 16 or 25 g alcohol kg À1 feed between days 7 and 19 of gestation. These alcohol exposures generate blood alcohol levels that correspond to low and moderate alcohol consumption and are lower than those that induce foetal alcohol syndrome. Serum oestradiol levels were elevated in pregnant rats exposed to alcohol (Po0.003). When adult, female offspring of alcohol-exposed dams developed significantly more 7,12-dimethylbenz[a]anthracene -induced mammary tumours, compared to the controls (tumour multiplicity; mean7s.e.m., controls: 2.070.3, 16 g alcohol: 2.770.4 and 25 g alcohol: 3.770.4; Po0.006). In addition, the mammary epithelial tree of the alcohol-exposed offspring was denser (Po0.004) and contained more structures that are susceptible for the initiation of breast cancer (Po0.001). Immunohistochemical assessment indicated that the mammary glands of 22-week-old in utero alcohol-exposed rats contained elevated levels of oestrogen receptor-a (Po0.04) that is consistent with the changes in mammary gland morphology. In summary, maternal alcohol intake during pregnancy increases female offspring's mammary tumorigenesis, perhaps by programming the foetal mammary gland to exhibit persistent alterations in morphology and gene expression. It remains to be determined whether an increase in pregnancy oestradiol levels mediated alcohol's effects on offspring's mammary tumorigenesis.

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“…9 However, recent data suggest that high birth weight and long gestational age among twins are risk factors for breast cancer but whether these would modify the comparisons to the singleton population remains to be established. [11][12][13] The studies in families with multiple twins showed no excess risks of cancer among twins. In one family with 3 twins and an excess of breast cancer, the risk is unlikely to be related to twinning.…”

Section: Discussionmentioning

confidence: 99%

Cancer risks in twins: Results from the Swedish family‐cancer database

Hemminki

2002

Intl Journal of Cancer

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Twin studies on cancer have addressed two general questions, one about the possible carcinogenic effects of twinning and the second about heritable effects of cancer. The first question is answered by comparing the occurrence of cancer in twins to that in singletons; the second is answered in probandwise analysis of monozygotic twins compared to dizygotic twins or siblings. We used the nationwide Swedish Family-Cancer Database on 10.2 million individuals and 62,574 0 -66-year-old twins to calculate standardized incidence ratios (SIRs) and 95% confidence intervals (CIs) for all main cancer compared to cancer in singletons. In probandwise analysis, the SIR was calculated for the co-twin of an affected twin. The overall risk of cancer in same or opposite sex twins was at the level of the risk for singletons. Testicular cancer was increased among same sex twins and all twins to an SIR of 1.43. Melanoma was decreased in these groups of twins to an SIR of 0.84. Some other cancer sites were increased or decreased in some groups of twins, but none in all twins. The SIR of breast cancer was 1.01 and 1.04 in same and opposite sex twins, respectively. Probandwise analysis showed increased risks for Hodgkin's disease in males and breast cancer and childhood acute lymphoid leukemia among females. The data on this unselected population of twins suggest that twinning per se is not a risk factor of cancer. However, because twins are smaller than singletons at birth, some possible effects could be masked by such differences. In utero hormonal exposures may be related to the risk of testicular cancer. The protective effects in melanoma may be due to socioeconomic factors.

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Birth characteristics and breast cancer risk: A study among like‐sexed twins

Cited by 48 publications

References 13 publications

Birth weight and risk of cancer

Birth weight and risk of cancer

In utero alcohol exposure increases mammary tumorigenesis in rats

Cancer risks in twins: Results from the Swedish family‐cancer database

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