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Perinatal and Familial Risk Factors for Soft-Tissue Sarcomas in Children, Adolescents, and Young Adults: A Population-Based Birth Cohort Study, Sweden, 1973-2012
Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper.
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2017 (Engelska)Ingår i: Pediatric Blood & Cancer, ISSN 1545-5009, E-ISSN 1545-5017, Vol. 64, s. S4-S5Artikel i tidskrift, Meeting abstract (Övrigt vetenskapligt) Published
Abstract [en]

Background/Objectives: Perinatal factors have been associated with soft-tissue sarcomas (STS) in case-control studies. However, (1) the specific contributions of factors including fetal growth remain unknown, (2) these factors have not been examined in large cohort studies, and (3) few assessments have evaluated risk in specific STS subtypes. Therefore, we sought to identify the role of perinatal and familial factors on the risk of STS in a large population-based birth cohort. Design/Methods: We identified 5,063,499 individuals in the Swedish Birth Registry born during 1973-2012. Subjects were linked to the Swedish Cancer Registry, where incident STS cases were identified. We evaluated perinatal and familial factors obtained from Statistics Sweden, including: fetal growth, gestational age, presence of a congenital anomaly, and parental age. Poisson regression was used to estimate incidence rate ratios (IRR) and 95% confidence intervals (CI) for associations between selected factors and STS overall, as well as by common subtypes. Results: There were 673 children, adolescents, and young adults diagnosed with STS in 77.5 million person-years of follow-up. Having a congenital anomaly was associated with STS risk (IRR=1.70, 95% CI: 1.23-2.35). This association was stronger (IRR=2.89, 95% CI: 1.25-6.70) in more recent years (2000-2012). High fetal growth was also associated with STS during the same time period (IRR=1.87, 95% CI: 1.06-3.30). Being born preterm (35 years) was inversely associated with the risk of developing synovial sarcoma (IRR=0.50, 95% CI: 0.26-0.94). Conclusions: In this cohort study, those with congenital anomalies and other adverse birth outcomes were more likely to develop a STS compared to their unaffected contemporaries. These associations may point to disrupted developmental pathways influencing the risk of STS. Our findings could implicate novel mechanisms underlying susceptibility to STS and may inform future surveillance, prevention, and treatment efforts.

Ort, förlag, år, upplaga, sidor
John Wiley & Sons, 2017. Vol. 64, s. S4-S5
Nationell ämneskategori
Cancer och onkologi Pediatrik
Identifikatorer
URN: urn:nbn:se:umu:diva-141796ISI: 000408978201004OAI: oai:DiVA.org:umu-141796DiVA, id: diva2:1161129
Konferens
49th Congress of the International Society of Paediatric Oncology (SIOP) Washington, DC, USA October 12–15, 2017
Anmärkning

Supplement: 3

Meeting Abstract: AW-04

Tillgänglig från: 2017-11-29 Skapad: 2017-11-29 Senast uppdaterad: 2018-06-09Bibliografiskt granskad

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Tavelin, BjörnMelin, BeatricePapworth, Karin

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Tavelin, BjörnMelin, BeatricePapworth, Karin
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Institutionen för strålningsvetenskaper
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Pediatric Blood & Cancer
Cancer och onkologiPediatrik

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