Genetic susceptibility to childhood leukaemia

Chokkalingam, Anand P.; Buffler, Patricia A.

doi:10.1093/rpd/ncn255

Cited by 31 publications

(24 citation statements)

References 69 publications

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“…As reported in a previous review [5], a search of the literature published prior to April 2008 identified 59 articles examining the association between variants of 36 different candidate gene loci and childhood ALL risk (blue bars in Fig. 1).…”

Section: Candidate Gene Association Studiesmentioning

confidence: 98%

“…Undetected associations due to insufficient sample sizes, which pertain to both genome-wide and candidate gene studies, is a central issue underscored by both the EncisoMora et al report [6] and previous reviews [5,104]. Power calculations have shown that even the largest GWAS conducted to date (907 cases and 2,398 controls) had limited ability to detect variants conferring relative risks of 1.4 or below and/or those with allele frequencies of \0.10 [6,104].…”

Section: Areas Of Ongoing and Future Workmentioning

confidence: 99%

“…Although a candidate gene study hoping to detect an SNP association with an allele frequency of 0.10 conferring a relative risk of 1.4 (assuming power = 0.80 and alpha = 0.05) would require fewer subjects, the sample size would still be substantial: about 600 cases and 600 controls. Furthermore, successful detection depends on whether the correct region and variants were selected a priori [5]. It is important to note, as well, that studies utilizing small sample sizes are sensitive to even small amounts of bias in genotyping or study design, potentially leading to erroneous results.…”

Section: Areas Of Ongoing and Future Workmentioning

confidence: 99%

“…The early age of onset of childhood ALL suggests that inherited genetic traits may play a role, and recent evidence indicates that these contribute to a substantial proportion of the variation in childhood ALL risk [5,6]. Such genetic traits can range from predisposing rare highly penetrant mutations to more common low penetrance genetic polymorphisms.…”

Section: Introductionmentioning

confidence: 99%

“…In this review, we focus our discussion on the most recent publications while referencing previous reviews and meta-analyses [5,[10][11][12]. Our objective is to provide the reader with an updated account of the current state of evidence regarding the genetic susceptibility to childhood ALL.…”

Section: Introductionmentioning

confidence: 99%

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Current evidence for an inherited genetic basis of childhood acute lymphoblastic leukemia

et al. 2012

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Acute lymphoblastic leukemia (ALL) is the most common cancer in children, and efforts to understand its etiology has followed a paradigm that common genetic variation in the presence of modifiable environmental factors contribute to disease risk. To date, there are numerous reports of candidate gene association studies suggesting an involvement of genetic loci in childhood ALL risk, but the general lack of consistency in results has underscored the need for careful interpretation and confirmation in additional well-designed studies. Complementary efforts using the genome-wide association study approach have shown indisputable evidence that common low penetrance genetic polymorphisms contribute to childhood ALL risk. However, current calculations show that these established disease loci only explain a portion of the total estimated contribution of common genetic variation on childhood ALL risk. Certain candidate gene loci previously examined likely contribute to this unexplained variation in risk, but the challenge moving forward will be to establish which ones based on the accumulating evidence. In this review, we describe the results of the most recent gene association studies in childhood ALL and discuss options for future efforts to advance this area of research.

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Section: Candidate Gene Association Studiesmentioning

confidence: 98%

Section: Areas Of Ongoing and Future Workmentioning

confidence: 99%

Section: Areas Of Ongoing and Future Workmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Current evidence for an inherited genetic basis of childhood acute lymphoblastic leukemia

et al. 2012

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Impact of high electromagnetic field levels on childhood leukemia incidence

Teepen

Dijck

2012

Intl Journal of Cancer

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The increasing exposure to electromagnetic fields (EMFs) has raised concern, as increased exposure may result in an increased risk of childhood leukemia (CL). Besides a short introduction of CL and EMF, our article gives an evaluation of the evidence of a causal relation between EMF and CL by critically appraising the epidemiological and biological evidence. The potential impact is also estimated by the population attributable risk. The etiology of CL is largely unknown, but is probably multifactorial. EMF may be one of the environmental exposures involved. Three pooled analyses of case–control studies showed a 1.4‐ to 1.7‐fold increased CL risk for extremely low‐frequency EMF (ELF‐EMF) exposure levels above 0.3 μT. Several biases may have played a role in these studies, but are unlikely to fully explain the increased risk. For effects of radiofrequency ELF evidence is lacking. None of the proposed biological mechanisms by which ELF‐EMF might cause CL have been confirmed. The estimated overall population attributable risk was 1.9%, with the highest estimates in Northern America and Brazil (4.2% and 4.1%, respectively). The potential impact of EMF exposure on public health is probably limited, although in some countries exposure might be relatively high and thus might have a more substantial impact. We recommend nationwide surveys to gain more insight into the contemporary exposure levels among children. Reducing exposure from power lines near densely populated areas and schools is advised. Future epidemiological studies should focus on limiting bias.

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Trends in childhood leukemia incidence over two decades from 1992 to 2013

Barrington‐Trimis

Cockburn

Metayer

et al. 2016

Intl Journal of Cancer

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Incidence rates of childhood leukemia in the United States have steadily increased over the last several decades, but only recently have disparities in the increase in incidence been recognized. In the current analysis, Surveillance, Epidemiology and End Results (SEER) data were used to evaluate recent trends in the incidence of childhood leukemia diagnosed at age 0–19 years from 1992–2013, overall and by age, race/ethnicity, gender, and histologic subtype. Hispanic White children were more likely than non-Hispanic White, non-Hispanic Black or non-Hispanic Asian children to be diagnosed with acute lymphocytic leukemia (ALL) from 2009–2013. From 1992–2013, a significant increase in ALL incidence was observed for Hispanic White children (annual percent change (APC)Hispanic=1.08, 95%CI:0.59, 1.58); no significant increase was observed for non-Hispanic White, Black or Asian children. ALL incidence increased by about 3% per year from 1992–2013 for Hispanic White children diagnosed from 15–19 years (APC=2.67; 95%CI:0.88, 4.49), and by 2% for those 10–14 years (APC=2.09; 95%CI:0.57, 3.63), while no significant increases in incidence were observed in non-Hispanic White, Black, or Asian children of the same age. Acute myeloid leukemia (AML) incidence increased among non-Hispanic White children under 1 year at diagnosis, and among Hispanic White children diagnosed at age 1–4. The increase in incidence rates of childhood ALL appears to be driven by rising rates in older Hispanic children (10–14, and 15–19 years). Future studies are needed to evaluate reasons for the increase in ALL among older Hispanic children.

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Genetic susceptibility to childhood leukaemia

Cited by 31 publications

References 69 publications

Current evidence for an inherited genetic basis of childhood acute lymphoblastic leukemia

Current evidence for an inherited genetic basis of childhood acute lymphoblastic leukemia

Impact of high electromagnetic field levels on childhood leukemia incidence

Trends in childhood leukemia incidence over two decades from 1992 to 2013

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