Prenatal and familial associations of testicular cancer

Swerdlow, Anthony; Huttly, Sharon; Smith, P. G.

doi:10.1038/bjc.1987.116

Cited by 106 publications

(107 citation statements)

References 22 publications

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“…However, exclusion of multiple births had no effect on the results. Contrary to previous suggestions British Journal of Cancer (1998) 77 (7), [1180][1181][1182][1183][1184][1185] C Cancer Research Campaign 1998 Testicular cancer risk and maternal parity 1185 Swerdlow et al, 1987;Braun et al, 1994;Braun et al, 1995), we found that multiple births tended to have a lower risk of testicular cancer than singletons. This finding, however, was based on a very limited number of cases.…”

Section: Materials and Methods Cohortcontrasting

confidence: 98%

“…Several case-control studies Swerdlow et al, 1987;Prener et al, 1992;M0ller and Skakkebek, 1996), but not all (Morrison, 1976;Henderson et al, 1979;Brown et al, 1986;Akre et al, 1996), have reported an increased risk of testicular cancer in first-born compared with later born sons. If such an association exists it suggests a modifying effect of environmental factors on the risk of testicular cancer (MacMahon and Pugh, 1970;Khoury et al, 1993), factors that are likely to be operational during fetal life or early childhood.…”

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confidence: 99%

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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 Cohortcontrasting

confidence: 98%

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confidence: 99%

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

Westergaard

Andersen²,

Pedersen³

et al. 1998

Br J Cancer

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“…26,27 Given the improvements in the standard of living for many populations over the past century, it is possible that some factors accompanying these changes in lifestyle is responsible for the increase in incidence. Increased maternal age and low parity have been suggested to be risk factors for testis cancer in some studies [28][29][30] and have also increased in prevalence in many populations over the past half-century. 31 These factors are known to be associated with the presence of elevated maternal estrogen levels during pregnancy, a condition hypothesized to increase the risk of abnormal gonadal development leading to testis cancer.…”

Section: Discussionmentioning

confidence: 99%

“…34,35 However, maternal smoking has not been linked to testis cancer risk in the majority of case-control studies conducted to date. 30,[36][37][38][39] Low birth weight and low gestational age have been reported in some studies to increase testis cancer risk. 29,36,40 With the improvements in recent decades in the survival of premature infants, 41 an increased frequency of testis cancers arising among survivors of premature birth may have contributed to an increase in testis cancer rates.…”

Section: Discussionmentioning

confidence: 99%

International patterns and trends in testis cancer incidence

Purdue

Devesa

Sigurdson

et al. 2005

Intl Journal of Cancer

200

148

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Although the incidence of testis cancer has risen markedly in many Western populations over the past half-century, it is not clear whether rates in other populations also have increased. To clarify this issue, we examined testis cancer incidence rates over the 25-year time period of 1973-1997 for selected populations around the world. Age-standardized incidence rates for 21 registries in the Americas, Asia, Europe and Oceania over successive 5-year time periods were obtained from volumes [4][5][6][7][8] Among many Western populations, testicular cancer incidence increased markedly over much of the past 20th century, 3,4 although recent data from some cancer registries suggest that rates may be plateauing. 5,6 A divergence in trends for different histologic subtypes of testis cancer has also been reported. The majority of testis cancers are germ-cell tumors, which are grouped histologically into seminomas and nonseminomas. 3 In Canadian and U.S. white populations, the incidence of nonseminoma has been increasing less rapidly than that of seminoma. 7,8 No adequate explanations for these trends have been identified, as the etiologies of these malignancies remain largely unknown.As investigations into secular trends of testis cancer have generally focused on populations of European ancestry, it is not clear whether rates in low-incidence populations also have increased over time. A study on international cancer trends between 1973-1987 by the International Agency for Research on Cancer (IARC) clearly demonstrated rising testis cancer rates in Japan and Puerto Rico but not in other low-incidence registries. 4 Since that time, IARC has published rates for additional time periods, enabling the analysis of secular trends over a longer time span. 2,9 To better understand how testis cancer incidence has changed over time across different populations, we examined incidence data over the 25-year period 1972-1997 from 21 populations in the Americas, Asia, Europe and Oceania. Material and methods Incidence dataTo examine the secular trends in the incidence of testis cancer (ICD-8, ICD-9 186), 10,11 age-standardized (World Population) 12,13 incidence rates in 21 populations were obtained from volumes 4-8 of Cancer Incidence in Five Continents (CI5). 2,9,14,15,16 The CI5 volumes include incidence data reported by selected populationbased cancer registries covering areas within Asia, Oceania, Africa, Europe and the Americas. Volumes 4-8 generally provided data for the 5-year time periods 1973-1977, 1978-1982, 1983-1987, 1988-1992 and 1993-1997, respectively. Rates for volumes 5-8 were based upon the ICD-9 classification of testis cancer, and volume 4 used the ICD-8 classification; there were no changes in the coding of testis cancer between the eighth and ninth ICD revisions. Incidence rates for different histologic subtypes of testis cancer (seminoma, nonseminoma, other/unspecified) were abstracted from volume 8.Populations were chosen for inclusion in our analysis on the basis of the following criteria: (i) the availability ...

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“…Moss et al (1985) and Swerdlow et al (1987) have reported an increase in breast cancer in mothers and lung cancer in parents of testicular cancer patients respectively in case-control studies. Similarly, there have been reports that testicular cancer may be part of the Li-Fraumeni syndrome (Hartley et al, 1989 There have been theories of hormonal imbalance in the mothers of patients as a cause of testicular cancer (Henderson et al, 1979).…”

mentioning

confidence: 98%