Maternal hormone levels in early gestation of cryptorchid males: a case-control study

Bernstein, Leslie; Pike, M. C.; Depue, RH; Ross, R. K.; Moore, J. W.; Be, Henderson

doi:10.1038/bjc.1988.223

Cited by 78 publications

(36 citation statements)

References 27 publications

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“…It has been hypothesized that high levels of endogenous oestrogens during critical stages of development in utero may increase the risk of cryptorchidism and testicular cancer (Henderson et al, 1979;, and at least three studies have found some evidence for increased oestrogen levels in first compared with later pregnancies (Bernstein et al, 1986;Panagiotopoulou et al, 1990;Key et al, 1996). Other studies also tend to support this hypothesis (McLachlan et al, 1975;Depue, 1984;Brown et al, 1986;Depue et al, 1983;Bernstein et al, 1988).…”

Section: Materials and Methods Cohortmentioning

confidence: 84%

Testicular cancer risk and maternal parity: a population-based cohort study

Westergaard

Andersen²,

Pedersen³

et al. 1998

Br J Cancer

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Summary The aim was to study, in a population-based cohort design, whether first-born sons run a higher risk of testicular cancer than later born sons; to investigate whether this difference in risk was affected by birth cohort, age of the son, maternal age, interval to previous delivery and other reproductive factors; and, finally, to evaluate to what extent changes in women's parity over time might explain the increasing incidence of testicular cancer. By using data from the Civil Registration System, a database was established of all women born in Denmark since 1935 and all their children alive in 1968 or born later. Sons with testicular cancer were identified in the Danish Cancer Registry. Among 1 015 994 sons followed for 15 981 967 person-years, 626 developed testicular cancer (443 non-seminomas, 183 seminomas). Later born sons had a decreased risk of testicular cancer (RR = 0.80, 95% Cl = 0.67-0.95) compared with first-born sons. The RR was 0.79 (95% Cl = 0.64-0.98) for non-seminomas and 0.81 (95% Cl = 0.58-1.13) for seminomas. There was no association between testicular cancer risk and overall parity of the mother, maternal or paternal age at the birth of the son, or maternal age at first birth. The decreased risk of testicular cancer among later born sons was not modified by age, birth cohort, interval to the previous birth, sex of the first-born child, or maternal age at birth of the son or at first birth. The increased proportion of first-borns from birth cohort 1946 to birth cohort 1969 only explained around 3% of an approximated two-fold increase in incidence between the cohorts. Our data document a distinctly higher risk of testicular cancer in firstborn compared with later born sons and suggest that the most likely explanation should be sought among exposures in utero. The increase in the proportion of first-borns in the population has only contributed marginally to the increase in testicular cancer incidence.

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Section: Materials and Methods Cohortmentioning

confidence: 84%

Testicular cancer risk and maternal parity: a population-based cohort study

Westergaard

Andersen²,

Pedersen³

et al. 1998

Br J Cancer

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“…Maoris have relatively lower birth weights than white individuals, and their mothers are frequently obese, which is associated with high estrogen levels. [90][91][92] Whereas timing of puberty has a strong association with the age at the peak incidence of testicular cancer, the correlation to cancers of other reproductive organs is less clear. A population-based, case-control study in Australia reported that markers of delayed androgen action, such as delayed growth spurt in puberty, were FIGURE 1 Age-adjusted incidence of testicular cancer related to activity of selected hormones.…”

Section: Testicular and Prostate Cancermentioning

confidence: 99%

Public Health Implications of Altered Puberty Timing

et al. 2008

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Changes in puberty timing have implications for the treatment of individual children, for the risk of later adult disease, and for chemical testing and risk assessment for the population. Children with early puberty are at a risk for accelerated skeletal maturation and short adult height, early sexual debut, potential sexual abuse, and psychosocial difficulties. Altered puberty timing is also of concern for the development of reproductive tract cancers later in life. For example, an early age of menarche is a risk factor for breast cancer. A low age at male puberty is associated with an increased risk for testicular cancer according to several, but not all, epidemiologic studies. Girls and, possibly, boys who exhibit premature adrenarche are at a higher risk for developing features of metabolic syndrome, including obesity, type 2 diabetes, and cardiovascular disease later in adulthood. Altered timing of puberty also has implications for behavioral disorders. For example, an early maturation is associated with a greater incidence of conduct and behavior disorders during adolescence. Finally, altered puberty timing is considered an adverse effect in reproductive toxicity risk assessment for chemicals. Recent US legislation has mandated improved chemical testing approaches for protecting children's health and screening for endocrinedisrupting agents, which has led to changes in the US Environmental Protection Agency's risk assessment and toxicity testing guidelines to include puberty-related assessments and to the validation of pubertal male and female rat assays for endocrine screening.

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“…An increased risk has also been reported for the contralateral descendent testis (Henderson et al 1979), suggesting common risk factors. Some prenatal risk factors seem to be common for both cryptorchidism and testicular cancer, such as high levels of estrogen in the first trimester (Bernstein et al 1988;Cosgrove et al 1977).…”

mentioning

confidence: 99%

Increased concentrations of polychlorinated biphenyls, hexachlorobenzene, and chlordanes in mothers of men with testicular cancer.

Hardell

Bavel

Lindström

et al. 2003

Environ Health Perspect

195

163

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An increasing incidence of testicular cancer has been reported from several countries in the Western world during the last decades. According to current hypothesis, testicular cancer is initiated during the fetal period, and exposure to endocrine disruptors, i.e., xenoestrogens, has been of concern. In this investigation we studied the concentrations of the sum of 38 polychlorinated biphenyls (PCBs), p,p´-dichlorodiphenyl-dichloroethylene, hexachlorobenzene (HCB), and chlordanes, in 61 cases with testicular cancer and 58 age-matched controls. Furthermore, case and control mothers were also asked to participate, and 44 case mothers and 45 control mothers agreed. They were of similar age. In cases only the concentration on lipid basis of cis-nonachlordane was significantly increased, whereas case mothers showed significantly increased concentrations of the sum of PCBs, HCB, trans-and cis-nonachlordane, and the sum of chlordanes. Among case mothers the sum of PCBs yielded an odds ratio (OR) of 3.8; 95% confidence interval (CI), 1.4-10 was calculated using the median concentration for the control mothers as cutoff value. For HCB, OR = 4.4 (95% CI, 1.7-12); for trans-nonachlordane, OR = 4.1 (95% CI, 1.5-11); for cis-nonachlordane, OR = 3.1 (95% CI, 1.2-7.8); and for sum of chlordanes, OR = 1.9 (95% CI, 0.7-5.0). No consistent different risk pattern was found for seminoma or nonseminoma testicular cancer.

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Maternal hormone levels in early gestation of cryptorchid males: a case-control study

Cited by 78 publications

References 27 publications

Testicular cancer risk and maternal parity: a population-based cohort study

Testicular cancer risk and maternal parity: a population-based cohort study

Public Health Implications of Altered Puberty Timing

Increased concentrations of polychlorinated biphenyls, hexachlorobenzene, and chlordanes in mothers of men with testicular cancer.

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