Childbearing at older age and endometrial cancer risk (Sweden)

Citation
M. Lambe et al., Childbearing at older age and endometrial cancer risk (Sweden), CANC CAUSE, 10(1), 1999, pp. 43-49
Citations number
41
Categorie Soggetti
Envirnomentale Medicine & Public Health
Journal title
CANCER CAUSES & CONTROL
ISSN journal
09575243 → ACNP
Volume
10
Issue
1
Year of publication
1999
Pages
43 - 49
Database
ISI
SICI code
0957-5243(199902)10:1<43:CAOAAE>2.0.ZU;2-D
Abstract
Objectives: Several studies have found an inverse association between older age at last birth and endometrial cancer risk. A nested case-control study was undertaken to examine the influence of this and other aspects of repro ductive patterns on the risk of developing endometrial cancer. Methods: Among women born in 1925 and later, 4,839 eligible patients were i dentified in the Swedish Cancer Register. For each case, five individually age-matched controls were randomly selected from a population-based Fertili ty Register. Relative risks were estimated from odds ratios obtained from c onditional logistic regression analyses. Results: Compared to uniparous women, childless women were at a higher risk of endometrial cancer (odds ratio [OR] = 1.38, 95% confidence interval [CI ] = 1.25-1.52). This association was stronger in younger (< 50 years) than in older (50 + years) women. At all ages of first birth, a delivery was ass ociated with a reduced risk of endometrial cancer that slowly diminished wi th time. Among parous women, the risk decreased by almost 20% for each addi tional live birth (OR = 0.81, CI = 0.78-0.84). In an analysis limited to wo men with two or more births that compared the independent effects of age at first and at last birth, only older age at last birth was associated with a lowered risk of endometrial cancer. The risk decreased at a rate of about 15% per five-year delay of last birth. Conclusions: Endometrial cancer is often referred to as the prototype hormo nally-determined disease in women. However, our findings give further suppo rt to the hypothesis that a birth may not only affect risk through hormonal influences, but possibly also through mechanical shedding of cells that ha ve undergone malignant transformation.