Tallness is associated with risk of testicular cancer: evidence for the nutrition hypothesis

Kp, Dieckmann; Hartmann, Jakob; Claßen, Johannes; Lüdde, R.; M, Diederichs; Pichlmeier, Uwe

doi:10.1038/sj.bjc.6604695

Cited by 30 publications

(20 citation statements)

References 45 publications

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“…For lipid level, we define risk alleles as variants that are positively associated with total cholesterol and LDL, the increased level of which is known to confer risk of heart disease, but negatively associated with HDL, the increased level for which is considered protective. For height, although such definitions are more ambiguous, we considered variants that are positively associated with height as a risk allele because increased mortality has been previously reported for taller subjects (16)(17)(18)(19).…”

Section: −30mentioning

confidence: 99%

Distribution of allele frequencies and effect sizes and their interrelationships for common genetic susceptibility variants

Park

Gail

Weinberg

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

274

229

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Recent discoveries of hundreds of common susceptibility SNPs from genome-wide association studies provide a unique opportunity to examine population genetic models for complex traits. In this report, we investigate distributions of various population genetic parameters and their interrelationships using estimates of allele frequencies and effect-size parameters for about 400 susceptibility SNPs across a spectrum of qualitative and quantitative traits. We calibrate our analysis by statistical power for detection of SNPs to account for overrepresentation of variants with larger effect sizes in currently known SNPs that are expected due to statistical power for discovery. Across all qualitative disease traits, minor alleles conferred "risk" more often than "protection." Across all traits, an inverse relationship existed between "regression effects" and allele frequencies. Both of these trends were remarkably strong for type I diabetes, a trait that is most likely to be influenced by selection, but were modest for other traits such as human height or late-onset diseases such as type II diabetes and cancers. Across all traits, the estimated effect-size distribution suggested the existence of increasingly large numbers of susceptibility SNPs with decreasingly small effects. For most traits, the set of SNPs with intermediate minor allele frequencies (5-20%) contained an unusually small number of susceptibility loci and explained a relatively small fraction of heritability compared with what would be expected from the distribution of SNPs in the general population. These trends could have several implications for future studies of common and uncommon variants.genetic prediction | missing heritability | population genetics L arge meta-analyses of genome-wide association studies (GWAS) have now identified more than 1,000 susceptibility loci for complex traits. Nevertheless, for most complex traits, the fraction of heritability explained by common variants remains below 10-15%, even for traits for which large numbers of loci have been detected [e.g., dozens to over 200 (1-3)]. We and others (4, 5) have projected that complex traits are likely to have an increasingly large number of susceptibility loci that have correspondingly smaller individual contributions to heritability. A fraction of these loci could be detected in future GWAS with large, but realistic, sample sizes, but they are still unlikely to fully explain a large fraction of missing heritability (4). The spectrum of genetic variation is greater than originally anticipated and suggests that the underlying genomic architecture of many diseases and traits could be more complex. Availability of newer-generation genotyping chips and sequencing technologies has raised the hope that future studies of uncommon and rare variants could increase the rate of discovery and explain an additional fraction of heritability, and eventually approach clinically useful discriminatory performance for genetic risk models.The discoveries generated from GWAS provide important insights ...

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Section: −30mentioning

confidence: 99%

Distribution of allele frequencies and effect sizes and their interrelationships for common genetic susceptibility variants

Park

Gail

Weinberg

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

274

229

View full text Add to dashboard Cite

show abstract

“…A number of studies have reported that increased adult height may be a risk factor for TC, thereby suggesting that factors related to adult height may also be related to risk of these tumors (Richiardi et al, 2007, Dieckmann et al, 2008, Lerro et al, 2010. Dieckmann et al (2008) found that very tall men (>195 cm) carried a TC risk of OR: 3.35 (95% confidence intervals (CI): 2.88-3.90; adjusted).…”

Section: Heightmentioning

confidence: 99%

“…Dieckmann et al (2008) found that very tall men (>195 cm) carried a TC risk of OR: 3.35 (95% confidence intervals (CI): 2.88-3.90; adjusted). In the STEED Study, there was a statistically significant increased risk of TC associated with greater height, and this association was particularly evident in men with seminomas (Lerro et al, 2010).…”

Section: Heightmentioning

confidence: 99%

Effect of endogenous and exogenous hormones on testicular cancer: the epidemiological evidence

Giannandrea¹,

Paoli

Figà–Talamanca

et al. 2013

Int. J. Dev. Biol.

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“…However, the Hamburg team around Dieckmann [1] reports no such fi ndings, and the hypothesis is further negated by other studies [8,9], whose results are, if anything, contrary.…”

Section: Discussionmentioning

confidence: 89%

Is testicular germ cell cancer associated with increased muscle mass or adiposity?

Gmeiner

Hruby

Nachbagauer

et al. 2011

Wien Klin Wochenschr

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According to the literature, patients with germ cell cancer of the testis on average show a higher body-mass-index (BMI) compared to a comparable group of equivalent age. The height of the umbilicus is a body region, where for adipose humans the amplitude increases markedly, hence for reference measurement appropriate. On the basis of the outcome of this thesis, the most probable explanation for the BMI rise is weight gain at other body parts.

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Tallness is associated with risk of testicular cancer: evidence for the nutrition hypothesis

Cited by 30 publications

References 45 publications

Distribution of allele frequencies and effect sizes and their interrelationships for common genetic susceptibility variants

Distribution of allele frequencies and effect sizes and their interrelationships for common genetic susceptibility variants

Effect of endogenous and exogenous hormones on testicular cancer: the epidemiological evidence

Is testicular germ cell cancer associated with increased muscle mass or adiposity?

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