© The Author 2007. Published by Oxford University Press.
CORRESPONDENCE |
Re: Prostate Cancer in Fathers With Fewer Male Offspring: the Jerusalem Perinatal Study Cohort
Affiliations of authors: Division of Molecular Genetic Epidemiology, German Cancer Research Centre, Heidelberg, Germany (JLB, KH); Center for Family and Community Medicine, Karolinska Institute, Huddinge, Sweden (JS, KH)
Correspondence to: Justo Lorenzo Bermejo, PhD, Division of Molecular Genetic Epidemiology, German Cancer Research Centre, Im Neuenheimer Feld 580, D-69120, Heidelberg, Germany (e-mail: j.lorenzo{at}dkfz.de).
We read with interest the recent article by Harlap et al. (1). The authors reported that, among 712 men with prostate cancer, those with only daughters had an increased risk of prostate cancer, compared with men with at least one son (adjusted relative risk = 1.40, 95% confidence interval [CI] = 1.20 to 1.64, P<.0001). The results prompted the authors to speculate that a Y chromosome locus may be involved in prostate cancer risk in the population they studied. Because the study of Harlap et al. was small, we decided to replicate the analyses taking advantage of the last update of the Swedish Family-Cancer Database.
The Database has been described in detail elsewhere (2,3). In our analyses, more than 3.1 million men were followed from birth of their first offspring, immigration date, or first year of the study (1961), whichever came latest, until death, diagnosis of any cancer, emigration, or December 31, 2004, whichever came first. We identified 120812 men with invasive prostate cancer diagnosed at the age of 32–99 years (median = 73 years), after 1–43 years of follow-up (median = 31 years). Standardized incidence ratios were used to estimate relative risks with the corresponding 95% confidence intervals and P values, according to number and sex of the offspring, and controlling for the covariates father's age (in 5-year age-groups: <20, 20–24, 25–29, ..., 80–84, 
85), father's age at start of follow-up (four equal-sized quartiles: <26, 26–30, 31–42, 42), socioeconomic index (six groups), father's year of birth (four equal-sized quartiles: <1920, 1920–1940, 1941–1955, after 1955) and calendar year (before 1965, 1965–1969, 1970–1974, ..., 1990–1994, 1995, 1996, ..., 2004). [After 1994, 1-year intervals were used because of a large increase in prostate cancer incidence in Sweden in this period (3,4).]
The 269720 offspring of the men diagnosed with prostate cancer included 51.09% males (95% CI = 50.90% to 51.28%). Despite the large sample size, this sex ratio was not statistically different (P = .15) from that of the offspring of men without prostate cancer (51.23% males, 95% CI = 51.19% to 51.26%). The estimated relative risks of prostate cancer for men with a variable number of sons are shown in Table 1. The only statistically significant finding was a 5% risk increase (95% CI = 1% to 9%) among men with three offspring but lacking sons. However, men without sons with four or more offspring were not at increased risk (P = .309). Replication of table 2 of the article of Harlap et al. revealed no trend for a decrease in the relative risk of prostate cancer as the number of sons increased (results not shown).
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The reasons for the inconsistencies between our data and the results from Harlap et al. are not clear. Although genetic heterogeneity related to the Y chromosome between the Swedish and the Jerusalem populations is possible, the size of our study, more than 150 times larger than that of Harlap et al., and the complete birth recording in the Database after 1961 may also suggest that the positive associations observed by Harlap et al. are explained by hidden misclassification or by chance. In addition, we note that these results agree with a Swedish ad hoc study on gender effects on familial cancer (5).
NOTES
Supported by Deutsche Krebshilfe, the Swedish Cancer Society, the Swedish Council for Working Life and Social Research, and the EU, LSHC-CT-2004-503465. The Family-Cancer Database was created by linking registers maintained at Statistics Sweden and the Swedish Cancer Registry.
REFERENCES
(1) Harlap S, Paltiel O, Friedlander Y, Calderon-Margalit R, Deutsch L, Kleinhaus KR, et al. Prostate cancer in fathers with fewer male offspring: the Jerusalem perinatal study cohort. J Natl Cancer Inst (2007) 99:77–81.
(2) Hemminki K, Li X, Plna K, Granström C, Vaittinen P. The nation-wide Swedish Family-Cancer Database: updated structure and familial rates. Acta Oncol (2001) 40:772–7.[CrossRef][Web of Science][Medline]
(3) Hemmminki K, Granström C, Sundquist J, Lorenzo Bermejo J. The updated Swedish Family-Cancer database used to assess familial risks of prostate cancer during rapidly increasing incidence. Hered Cancer Clin Pract (2006) 4:186–92.
(4) Hemminki K, Rawal R, Lorenzo Bermejo J. Prostate cancer screening, changing age-specific incidence trends and implications on familial risk. Int J Cancer (2005) 113:312–5.[CrossRef][Web of Science][Medline]
(5) Hemminki K, Li X. Gender effects in familial cancer. Int J Cancer (2002) 102:184–7.[CrossRef][Web of Science][Medline]
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J Natl Cancer Inst 2007 99: 77-81.
J Natl Cancer Inst 2007 99: 903-904.
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