Effects of the Y chromosome on quantitative growth: An anthropometric study of 47,XYY males

Varrela, Juha; Alvesalo, Lassi

doi:10.1002/ajpa.1330680211

Cited by 23 publications

(9 citation statements)

References 26 publications

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“…There are common features of the abnormality, including increased growth (Varrela and Alvesalo 1985;Alvesalo 1997), tall stature (RatcliVe 1994) and nodulocystic acne (Voorhees et al 1970), but these are consequences, rather than a cause of the abnormality.…”

Section: Discussionmentioning

confidence: 96%

Mortality and cancer incidence in males with Y polysomy in Britain: a cohort study

Higgins¹,

Swerdlow²,

Schoemaker³

et al. 2007

Hum Genet

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The mortality and cancer incidence risks among males with Y polysomy are unknown because there have been no large long-term cohort studies carried out of such men. We conducted a cohort study of 667 men diagnosed with the abnormality in Britain since 1959 to compare their mortality and cancer incidence rates with those of the general population. Sixty deaths occurred during follow-up to December 2005, twice the number expected from general population rates (standardised mortality ratio (SMR) = 2.0 (95% confidence interval (CI) 1.5-2.6)). Significantly raised mortality was observed for diseases of the nervous system (SMR = 7.0, 95% CI: 2.3-16.4), circulatory system (SMR = 2.1, 95% CI: 1.3-3.2), respiratory system (SMR = 4.0, 95% CI: 1.8-7.5), genitourinary system (SMR = 10.2, 95% CI: 1.2-36.9), and congenital anomalies (SMR = 11.9, 95% CI: 3.2-30.5). Four of the five nervous system deaths were from epilepsy, the risk of death from this condition being more than 20-fold raised. The rates of cancer incidence and mortality among these men was not significantly different from those in the general population. This study provides evidence that mortality rates from several specific causes are raised among men with Y polysomy. The use of these data in genetic counselling should be cautious particularly for cases of Y polysomy that are detected prenatally. Further investigations are required to confirm these findings and to elucidate the possible role of genes on the Y chromosome in the aetiology of these causes of death.

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Section: Discussionmentioning

confidence: 96%

Mortality and cancer incidence in males with Y polysomy in Britain: a cohort study

Higgins¹,

Swerdlow²,

Schoemaker³

et al. 2007

Hum Genet

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“…Traditionally, the Y chromosome has been considered to be genetic 'desert', with few active genes, but recent research (58) has overturned this view, providing evidence that a number of genes crucial to growth and development occur on the Y chromosome (59). The presence of extra Y chromosomes is associated with high growth rates and large size (60). Burgoyne (61) demonstrated that genes on the Y chromosome cause rapid growth of XY embryos relative to XX embryos prior to implantation in mice.…”

Section: Selfish Sex Chromosomesmentioning

confidence: 99%

Intragenomic conflict and cancer

2002

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Summary Intragenomic conflict occurs when some elements within the genome produce effects that enhance their own probability of replication or transmission at the expense of other elements within the same genome. Here it is proposed that mutations involved in intragenomic conflict are particularly likely to be co-opted by evolving lineages of cancer cells, and hence should be associated with the occurrence of cancer. We discuss several types of intragenomic conflict that are associated with various forms of cancer. ª

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“…XYY humans are male and typically taller than the average (Varrela & Alvesalo, 1985;Ogata & Matsuo, 1993). Effects on growth assayed by tooth size in XYY individuals also provide direct evidence of a Y effect on tissue growth (Alvesalo eta!., 1985;Townsend & Alvesalo, 1985).…”

Section: Introductionmentioning

confidence: 99%

Embryonic growth and the evolution of the mammalian Y chromosome. I. The Y as an attractor for selfish growth factors

Hurst¹

1994

Heredity

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The fitness of a mammalian zygote is affected by its probability of implantation and of postimplantation maintenance as well as the level of transplacental and transmammary uptake of resources. As with paternally expressed imprinted genes, in a species in which females are not obligately monogamous, a Y-linked sequence that can positively alter any of the above parameters could spread in a population even if it harms the prospects of other embryos. Such a selfish Y-linked gene could act as a sex ratio distorter. In contrast to autosomal imprinted loci, the patrilineal inheritance of the Y ensures that selfish Y-linked growth-promoting genes need not evolve a means to ensure correct parent-dependent expression rules. Thus, as the conditions for both their initial evolution and spread are relatively relaxed, the mammalian Y chromosome is expected to be an attractor for growth-promoting genes. Data from mice and humans indicate that, as expected and in contrast to the Y of flies, the mammalian Y harbours growth factors, sex ratio factors and multiple foetally expressed genes. The accumulation of Y-linked genes may also be explained in terms of sexual antagonism. Sexual antagonism and the model presented here are not mutually exclusive

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Effects of the Y chromosome on quantitative growth: An anthropometric study of 47,XYY males

Cited by 23 publications

References 26 publications

Mortality and cancer incidence in males with Y polysomy in Britain: a cohort study

Mortality and cancer incidence in males with Y polysomy in Britain: a cohort study

Intragenomic conflict and cancer

Embryonic growth and the evolution of the mammalian Y chromosome. I. The Y as an attractor for selfish growth factors

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