Neonatal medical exposures and characteristics of low birth weight hepatoblastoma cases: A report from the Children's Oncology Group

Turcotte, Lucie M.; Georgieff, Michael; Ross, Julie A.; Feusner, James; Tomlinson, Gail E.; Malogolowkin, Marcio H.; Krailo, Mark; Miller, Nicole; Fonstad, Rachel; Spector, Logan G.

doi:10.1002/pbc.25128

Cited by 41 publications

(35 citation statements)

References 30 publications

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“…Details of the study design have been published previously. (6–8) Briefly, cases were recruited from United States COG institutions and included children diagnosed with hepatoblastoma (International Classification of Childhood Cancers histology code 8970) prior to 15 years of age between January 1, 2000 and December 31, 2008. Other inclusion criteria include birth in the United States, birth mother available for interview who speaks English or Spanish, and physician permission to contact cases.…”

Section: Methodsmentioning

confidence: 99%

Maternal and paternal occupational exposures and hepatoblastoma: results from the HOPE study through the Children’s Oncology Group

Janitz

Ramachandran

Tomlinson³

et al. 2017

J Expo Sci Environ Epidemiol

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Introduction Little is known about the etiology of hepatoblastoma. We aimed to confirm the results of a previous study evaluating the association between parental occupational exposures and hepatoblastoma. Methods In our case-control study, we identified cases (n=383) from the Children’s Oncology Group and controls from birth certificates (n=387), which were frequency matched to cases on year and region of birth, sex, and birth weight. Occupational exposure in the year prior to and during the index pregnancy was collected through maternal interview and analyzed using unconditional logistic regression. Results The odds of both paternal and maternal “Likely” exposure to paints was elevated among cases compared to controls (Paternal Odds Ratio [OR]: 1.71, 95% Confidence Interval [CI]: 1.04, 2.81; Maternal OR: 3.29, 95% CI: 0.32, 33.78) after adjustment for matching factors and the confounding factors of maternal race (maternal only) and household income. In addition, paternal exposure to other chemicals was also elevated when adjusting for matching factors only (OR: 1.53, 95% CI: 1.02, 2.30). Discussion The results of our study provide further evidence of an association between parental occupation and hepatoblastoma. These results warrant further investigation of the etiologically relevant timing of occupational exposure to fumes and chemicals related to hepatoblastoma.

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Section: Methodsmentioning

confidence: 99%

Maternal and paternal occupational exposures and hepatoblastoma: results from the HOPE study through the Children’s Oncology Group

Janitz

Ramachandran

Tomlinson³

et al. 2017

J Expo Sci Environ Epidemiol

View full text Add to dashboard Cite

show abstract

“…The reasons behind the association of higher birth weight with childhood cancers have not been explored in detail, but may include prenatal growth hormone exposure (43), the underlying genetics of birth weight (44), and the greater number of cells at risk for carcinogenic transformation. The strong inverse association of hepatoblastoma with birth weight has been thought to be related to neonatal treatment, but no culprit exposure has been identified to date(45). …”

Section: Introductionmentioning

confidence: 99%

Genetic and Nongenetic Risk Factors for Childhood Cancer

Spector

Pankratz

Marcotte

2015

Pediatric Clinics of North America

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162

169

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Summary The causes of childhood cancer have been systematically studied for several decades, but apart from high-dose radiation and prior chemotherapy there are few or no strong external risk factors. On the other hand, inherent risk factors including birth weight, parental age, and congenital anomalies are consistently associated with most types of pediatric cancer. Rare, highly-penetrant syndromes have long been known to cause a small proportion of cancers but recently the contribution of common genetic variation to etiology has come into focus through genome wide association studies. These have highlighted genes not previously implicated in childhood cancers and, surprisingly, have suggested that common variation explains a larger proportion of childhood cancers than adult. Rare variation and non-Mendelian inheritance, such as through maternal genetic effects or de novo germline mutations, may also contribute to childhood cancer risk but have not been widely examined to date.

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“…As reflected by the controlled direct effect estimates from a marginal structural model, the association between maternal preeclampsia and hepatoblastoma can be partly explained by mediation by NICU attendance and the intensive medical care associated with it. A previous investigation identified di‐(2‐ethylhexyl) phthalate (DEHP), a commonly applied plasticizer in medical devices and tubing, as a rodent hepatocarcinogen . Infants going through intensive and long‐term medical interventions such as mechanical ventilation and oxygen therapy are more likely to be exposed to high cumulative doses of DEHP which have tumourigenic effects on the immature liver …”

Section: Commentmentioning

confidence: 99%

Maternal Preeclampsia and Odds of Childhood Cancers in Offspring: A California Statewide Case–Control Study

Ritz

Cockburn

et al. 2017

Paediatric Perinatal Epid

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Background Preeclampsia is a major cause of adverse effects on fetal health. We examined associations between fetal exposure to preeclampsia and subsequent odds of childhood cancers. Methods We obtained childhood cancer cases (n=13,669) diagnosed at five years old or younger between 1988 and 2012 from the California Cancer Registry and linked them to birth certificates. Controls (n=271,383) were randomly selected from all California births and frequency matched to cases by birth year. We obtained data regarding preeclampsia during pregnancy, labour, and delivery from the medical worksheet of the electronic birth record. We used unconditional logistic regression models with stabilised inverse probability weights to estimate the effect of preeclampsia on each subtype of childhood cancer, taking into account potential confounding by pregnancy characteristics. Marginal structural models were fitted to assess the controlled direct effects of preeclampsia, independent of preterm delivery and NICU admission. Results Although a null association was observed for all cancer subtypes combined (odds ratio (OR) 1.0, 95% confidence interval (CI) 0.9, 1.2), preeclampsia was found to be associated with increased odds of two histologic subtypes of germ cell tumours: seminomas (OR 8.6, 95% CI 1.9, 38.4) and teratoma (OR 3.0, 95% CI 1.7, 5.4), but not yolk sac tumours in children. Odds remained elevated after adjusting for preterm delivery and NICU admission. Increases in odds were also observed for hepatoblastoma, however this association was attenuated in marginal structural models after accounting for NICU admission. Conclusions These findings suggest that maternal preeclampsia is associated with higher odds of some rare childhood cancers and may shed light on new aetiologic factors for these cancers.

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Neonatal medical exposures and characteristics of low birth weight hepatoblastoma cases: A report from the Children's Oncology Group

Cited by 41 publications

References 30 publications

Maternal and paternal occupational exposures and hepatoblastoma: results from the HOPE study through the Children’s Oncology Group

Maternal and paternal occupational exposures and hepatoblastoma: results from the HOPE study through the Children’s Oncology Group

Genetic and Nongenetic Risk Factors for Childhood Cancer

Maternal Preeclampsia and Odds of Childhood Cancers in Offspring: A California Statewide Case–Control Study

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