Fetal growth and the risk of childhood non-CNS solid tumours in Western Australia

Laurvick, Crystal L.; Milne, Elizabeth; Blair, Eve; Klerk, Nicholas de; Charles, Adrian; Bower, Carol

doi:10.1038/sj.bjc.6604424

Cited by 18 publications

(25 citation statements)

References 17 publications

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“…We and others have not only shown that high birth weight increases the risk of RMS thereby extending the associations reported for childhood cancers, including leukaemia (Caughey and Michels, 2009), brain tumours (Harder et al, 2008) and Wilms tumour (Schuz et al, 2001), but also directly linked it to the extent of growth in utero. Our study supports the view that size for gestational age provides insight beyond that of birth weight per se (Laurvick et al, 2008) and can identify new high-risk groups (Schuz et al, 2001). We observed no association between gestational age and RMS risk, which may also reflect the fact that only 26 embryonal and 7 alveolar RMS cases were born prematurely, spread across 5 weeks before term (32 -36 weeks), whereas only two RMS cases were born very prematurely (more than 5 weeks).…”

Section: Discussionsupporting

confidence: 65%

“…This is the first study to show that accelerated in utero growth, measured by higher than expected weight for gestational age, increases the risk of embryonal RMS. The only previous study of relevance suggested an increased risk with increasing birth weight and intrauterine growth (Laurvick et al, 2008), but the small sample size precluded precise estimates. We and others have not only shown that high birth weight increases the risk of RMS thereby extending the associations reported for childhood cancers, including leukaemia (Caughey and Michels, 2009), brain tumours (Harder et al, 2008) and Wilms tumour (Schuz et al, 2001), but also directly linked it to the extent of growth in utero.…”

Section: Discussionmentioning

confidence: 99%

“…High birth weight has been associated with several childhood malignancies, and recent evidence suggests that accelerated intrauterine growth may increase RMS risk, although based on only 27 cases (Laurvick et al, 2008). Further, the two major histological subtypes (embryonal and alveolar RMS) have distinct localisations, ages of onset, incidence and survival trends (Ries, 1999;Ognjanovic et al, 2009) and distinct tumour gene expression signatures (Davicioni et al, 2006;Wachtel et al, 2006;Lae et al, 2007), suggesting that their aetiologies may be distinct.…”

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confidence: 99%

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Birth characteristics and the risk of childhood rhabdomyosarcoma based on histological subtype

et al. 2009

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BACKGROUND: Little is known about risk factors for childhood rhabdomyosarcoma (RMS) and the histology-specific details are rare. METHODS: Case -control studies formed by linking cancer and birth registries of California, Minnesota, New York, Texas and Washington, which included 583 RMS cases (363 embryonal and 85 alveolar RMS) and 57 966 randomly selected control subjects, were analysed using logistic regression. The associations of RMS (overall, and based on embryonal or alveolar histology) with birth weight across five 500 g categories (from 2000 to 4500 g) were examined using normal birth weight (2500 -3999 g) as a reference. Large (490th percentile) and small (o10th percentile) size for gestational age were calculated based on birth weight distributions in controls and were similarly examined. RESULTS: High birth weight increased the risk of embryonal RMS and RMS overall. Each 500 g increase in birth weight increased the risk of embryonal RMS (odds ratio (OR) ¼ 1.27, 95% confidence interval (CI) ¼ 1.14 -1.42) and RMS overall (OR ¼ 1.18, 95% CI ¼ 1.09 -1.29). Large size for gestational age also significantly increased the risk of embryonal RMS (OR ¼ 1.42, 95% CI ¼ 1.03 -1.96). CONCLUSIONS: These data suggest a positive association between accelerated in utero growth and embryonal RMS, but not alveolar RMS. These results warrant cautious interpretation owing to the small number of alveolar RMS cases.

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Section: Discussionsupporting

confidence: 65%

Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Birth characteristics and the risk of childhood rhabdomyosarcoma based on histological subtype

et al. 2009

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“…An indirect link between imprinting and childhood cancer comes from the association between higher birth weight, accelerated fetal growth, and higher rates of most of the major childhood cancers (17)(18)(19)(20)(21). To the extent that perturbations to imprinting can lead to misregulated growth, this association between growth and cancer may also link misregulated imprinting to cancer.…”

Section: Growth Pathologies: Cancermentioning

confidence: 99%

Pathology from evolutionary conflict, with a theory of X chromosome versus autosome conflict over sexually antagonistic traits

Frank

Crespi

2011

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

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Evolutionary conflicts cause opponents to push increasingly hard and in opposite directions on the regulation of traits. One can see only the intermediate outcome from the balance of the exaggerated and opposed forces. Intermediate expression hides the underlying conflict, potentially misleading one to conclude that trait regulation is designed to achieve efficient and robust expression, rather than arising by the precarious resolution of conflict. Perturbation often reveals the underlying nature of evolutionary conflict. Upon mutation or knockout of one side in the conflict, the other previously hidden and exaggerated push on the trait may cause extreme, pathological expression. In this regard, pathology reveals hidden evolutionary design. We first review several evolutionary conflicts between males and females, including conflicts over mating, fertilization, and the growth rate of offspring. Perturbations of these conflicts lead to infertility, misregulated growth, cancer, behavioral abnormalities, and psychiatric diseases. We then turn to antagonism between the sexes over traits present in both males and females. For many traits, the different sexes favor different phenotypic values, and constraints prevent completely distinct expression in the sexes. In this case of sexual antagonism, we present a theory of conflict between X-linked genes and autosomal genes. We suggest that dysregulation of the exaggerated conflicting forces between the X chromosome and the autosomes may be associated with various pathologies caused by extreme expression along the male-female axis. Rapid evolution of conflicting X-linked and autosomal genes may cause divergence between populations and speciation.genomic imprinting | disease risk | intragenomic conflict | human genetics P athologies often arise from perturbations of evolutionary conflict. In conflict between different components of the genome, the opposing genes push in opposite directions on a particular trait, such as sex ratio or offspring growth rate (1). The regulation of such traits under conflict becomes dominated by a balance of opposing forces. This precarious regulatory balance contrasts with the typically supposed design of regulation to achieve efficient and robust expression (2, 3). Mutation or knockout of one side in the conflict leads to the other side dominating expression, often pushing the trait to an extreme in the absence of the opposing force. Extreme expression typically causes pathology.In this paper, we develop the idea of pathology arising from perturbations to evolutionary conflicts. We discuss several examples of evolutionary conflicts, the ways in which conflict may lead to exaggerated opposition of forces on a trait, and the occasional breakdown in the normal balance of opposing forces that leads to pathology. We also present a theory of evolutionary conflict between X-linked and autosomal genes over traits that differ in their consequences for male and female fitness. Perturbations to the Xautosome conflict may lead to pathologies of extreme exp...

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“…Several studies have looked at various birth characteristics and especially high birth weight has been associated with an increased risk of Wilms tumor with some degree of consistency. [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] Wilms tumor patients with either Beckwith-Wiedemann syndrome or hemihypertrophy were found to have high birth weights, but a positive association was also seen among children with no other congenital abnormalities. 5 Two studies reported that the association between high birth weight and Wilms tumor was stronger in patients with perilobar nephrogenic rests (PLNR) than in patients with intralobar nephrogenic rests (ILNR), 6,7 whereas the presence of PLNR was associated with loss of imprinting of IGF2, [24][25][26] suggesting that patients with this loss of imprinting account for the birth weight association.…”

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confidence: 99%

Birth characteristics and Wilms tumors in children in the Nordic countries: A register‐based case–control study

Schüz

Schmidt

Kogner

et al. 2011

Intl Journal of Cancer

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Little is known about causes of Wilms tumor. Because of the young age at diagnosis, several studies have looked at various birth characteristics. We conducted a registry-based case-control study involving 690 cases of Wilms tumor aged 0-14 years, occurring in Denmark, Finland, Norway or Sweden during 1985, individually matched to five controls drawn randomly from the Nordic childhood population. Information on birth characteristics was obtained from the population-based medical birth registries. We estimated odds ratios (ORs) and 95% confidence intervals (CIs) using conditional logistic regression analysis. We observed a distinct association between Wilms tumor and high birth weight (4 kg) for girls (OR 1.97, CI 1.50-2.59) but not for boys (1.04, 0.78-1.38); overall, the OR was 1.43 (1.17-1.74). Among girls, risk increased by 28% (15-42%) per 500 g increase in birth weight. Large-for-gestational age girls also had a higher risk (2.48, 1.51-4.05), whereas no effect was seen for boys (1.12, 0.60-2.07). An association was seen with Apgar score at 5 min < 7 for both sexes combined (5.13, 2.55-10.3). ORs close to unity were seen for parental age and birth order. In our large-scale, registry-based study, we confirmed earlier observations of an association between high birth weight and risk of Wilms tumor, but we found an effect only in girls. The higher risk of infants with low Apgar score might reflect hypoxia causing cell damage, adverse side effects of neonatal treatment or reverse causation as low Apgar score might indicate the presence of a tumor.Renal tumors in children are rare. Its major subtype, Wilms tumor or nephroblastoma, constituting >95% of all childhood renal tumors, is an embryonal malignancy arising from remnants of the immature kidney.

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Fetal growth and the risk of childhood non-CNS solid tumours in Western Australia

Cited by 18 publications

References 17 publications

Birth characteristics and the risk of childhood rhabdomyosarcoma based on histological subtype

Birth characteristics and the risk of childhood rhabdomyosarcoma based on histological subtype

Pathology from evolutionary conflict, with a theory of X chromosome versus autosome conflict over sexually antagonistic traits

Birth characteristics and Wilms tumors in children in the Nordic countries: A register‐based case–control study

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