A possible link between the pubertal growth of girls and ovarian cancer in their daughters.

A possible link between the pubertal growth of girls and ovarian cancer in their daughters.
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DOI:
10.1002/ajhb.20789
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发表时间:
2008-11
期刊:
American journal of human biology : the official journal of the Human Biology Council
影响因子:
--
通讯作者:
Eriksson JG
Eriksson JG
中科院分区:
其他
文献类型:
--
作者:
Barker DJ;Osmond C;Thornburg KL;Kajantie E;Eriksson JG

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在青春期,女性骨盆的髂嵴之间的距离(通过嵴间和棘间直径测量)迅速增加。这主要由雌激素控制。我们对1934-1944年间出生于赫尔辛基的6,370名妇女进行了随访,这些妇女的母亲在常规产前检查中测量了骨盆骨。我们以前曾报道过,母亲的嵴间直径较大的妇女患乳腺癌的几率较高。我们推测,大的嵴间直径是高循环雌激素浓度的标志,这是在青春期建立,持续通过生殖生活,并导致遗传不稳定性分化的乳腺细胞在女性胚胎。我们现在报告同一队列中的卵巢癌。我们的假设是,这种癌症的风险也会更高的妇女,其母亲有更广泛的臀部。我们发现,与所有其他女性相比,棘突间直径大于27 cm的母亲的女儿患卵巢癌的风险比为3.3(95%CI 1.6-7.0,P = 0.004)。在初潮早的母亲中,每一项宽臀的测量都与女儿患卵巢癌的风险增加有关。我们推测卵巢癌是由胎儿卵巢暴露于母体性激素而引发的。这些激素的浓度可能在初潮早的母亲中更高。引发卵巢癌的母体性激素谱可能是儿童早期营养不良和生长的产物,随后是青春期前的追赶性生长。
At puberty, the distance between the iliac crests of the female pelvis, measured by the intercristal and interspinous diameters, increases rapidly. This is mainly controlled by estrogens. We have followed up 6,370 women who were born in Helsinki during 1934–1944, and whose mothers’ pelvic bones were measured during routine antenatal care. We have previously reported that women whose mothers had larger intercristal diameters had higher rates of breast cancer. We postulated that large intercristal diameters are markers of high circulating concentrations of estrogen, which are established at puberty, persist through reproductive life and cause genetic instability in differentiating breast cells in female embryos. We now report on ovarian cancer in the same cohort. Our hypothesis was that the risk of this cancer would also be higher in women whose mothers had broader hips. We found that, when compared with all other women, the hazard ratio for ovarian cancer was 3.3 (95% CI 1.6–7.0, P = 0.004) in the daughters of mothers whose interspinous diameter was greater than 27 cm. Among mothers who had an early menarche, each measure of broad hips was associated with increased risk of ovarian cancer in their daughters. We postulate that ovarian cancer is initiated by exposure of the fetal ovary to maternal sex hormones. Concentrations of these hormones may be higher in mothers who had an early menarche. The maternal sex hormone profile that initiates ovarian cancer may be the product of poor nutrition and growth in early childhood followed by catch-up pre-pubertal growth.