Maternal Diet and Infant Leukemia: The DNA Topoisomerase II Inhibitor Hypothesis: A Report from the Children's Oncology Group

Spector, Logan G.; Xie, Yang; Robison, Leslie L.; Heerema, Nyla A.; Hilden, Joanne M.; Lange, Beverly J.; Felix, Carolyn A.; Davies, Stella M.; Slavin, Joanne L.; Potter, John D.; Blair, Cindy K.; Reaman, Gregory H.; Ross, Julie A.

doi:10.1158/1055-9965.epi-04-0602

Cited by 184 publications

(152 citation statements)

References 34 publications

Supporting

Mentioning

147

Contrasting

Unclassified

Order By: Relevance

“…Eligibility criteria for cases included: (1) diagnosis with acute leukaemia in the first year of life between 1 January 1996 and 20 August 2002; (2) an Englishspeaking biological mother available for a telephone interview and (3) no Down syndrome. Controls were identified and contacted by random digit dialling (RDD) (for more details see Spector et al, 2005).…”

Section: Methodsmentioning

confidence: 99%

Maternal hemoglobin concentration during pregnancy and risk of infant leukaemia: a children's oncology group study

et al. 2006

View full text Add to dashboard Cite

show abstract

Section: Methodsmentioning

confidence: 99%

Maternal hemoglobin concentration during pregnancy and risk of infant leukaemia: a children's oncology group study

et al. 2006

View full text Add to dashboard Cite

show abstract

“…Even though genistein and other bioflavonoids appear to be chemopreventative in adults, the maternal consumption (during pregnancy) of foods that are naturally high in these topoisomerase II poisons increases the risk of developing these infant leukemias more than 3-fold [148]. Once again, chromosomal breakpoints in these leukemias are proximal to topoisomerase II cleavage sites [149].…”

Section: Non-covalent Topoisomerase II Poisonsmentioning

confidence: 99%

DNA topoisomerase II, genotoxicity, and cancer

McClendon

Osheroff

2007

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

359

466

View full text Add to dashboard Cite

Type II topoisomerases are ubiquitous enzymes that play essential roles in a number of fundamental DNA processes. They regulate DNA under-and overwinding, and resolve knots and tangles in the genetic material by passing an intact double helix through a transient double-stranded break that they generate in a separate segment of DNA. Because type II topoisomerases generate DNA strand breaks as a requisite intermediate in their catalytic cycle, they have the potential to fragment the genome every time they function. Thus, while these enzymes are essential to the survival of proliferating cells, they also have significant genotoxic effects. This latter aspect of type II topoisomerase has been exploited for the development of several classes of anticancer drugs that are widely employed for the clinical treatment of human malignancies. However, considerable evidence indicates that these enzymes also trigger specific leukemic chromosomal translocations. In light of the impact, both positive and negative, of type II topoisomerases on human cells, it is important to understand how these enzymes function and how their actions can destablize the genome. This article discusses both aspects of human type II topoisomerases.

show abstract

“…There is no doubt that the risks of developing early acute leukemia are modulated by complex interactions between inherited predispositions, environmental exposure to damaging agents and chance events (28,34). Despite the fact that such leukemias are very rare, their investigation is absolutely necessary for the study of leukemogenesis because they have a short latency period together with the known immune molecular markers.…”

Section: Molecular and Exploratory Epidemiology What Makes These Leukmentioning

confidence: 99%

Acute leukemia in early childhood

Emerenciano

Koifman

Pombo‐de‐Oliveira

2007

Braz J Med Biol Res

View full text Add to dashboard Cite

Acute leukemia in early childhood is biologically and clinically distinct. The particular characteristics of this malignancy diagnosed during the first months of life have provided remarkable insights into the etiology of the disease. The pro-B, CD10 negative immunophenotype is typically found in infant acute leukemia, and the most common genetic alterations are the rearrangements of the MLL gene. In addition, the TEL /AML1 fusion gene is most frequently found in children older than 24 months. A molecular study on a Brazilian cohort (age range 0-23 months) has detected TEL /AML1 +ve (N = 9), E2A/PBX1 +ve (N = 4), PML /RARA +ve (N = 4), and AML1/ETO +ve (N = 2) cases. Undoubtedly, the great majority of genetic events occurring in these patients arise prenatally. The environmental exposure to damaging agents that give rise to genetic changes prenatally may be accurately determined in infants since the window of exposure is limited and known. Several studies have shown maternal exposures that may give rise to leukemogenic changes. The Brazilian Collaborative Study Group of Infant Acute Leukemia has found that mothers exposed to dipyrone, pesticides and hormones had an increased chance to give birth to babies with infant acute leukemia [OR = 1.48 (95%CI = 1.05-2.07), OR = 2.27 (95%CI = 1.56-3.31) and OR = 9.08 (95%CI = 2.95-27.96)], respectively. This review aims to summarize recent clues that have facilitated the elucidation of the biology of early childhood leukemias, with emphasis on infant acute leukemia in the Brazilian population.

show abstract

Maternal Diet and Infant Leukemia: The DNA Topoisomerase II Inhibitor Hypothesis: A Report from the Children's Oncology Group

Cited by 184 publications

References 34 publications

Maternal hemoglobin concentration during pregnancy and risk of infant leukaemia: a children's oncology group study

Maternal hemoglobin concentration during pregnancy and risk of infant leukaemia: a children's oncology group study

DNA topoisomerase II, genotoxicity, and cancer

Acute leukemia in early childhood

Contact Info

Product

Resources

About