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Promoter SNPs in G1/S checkpoint regulators and their impact on the susceptibility to childhood leukemia.

Abstract：

:Mutations leading to the alteration of cell-cycle checkpoint functions are a common feature of most cancers. Because of the highly regulated nature of the cell cycle, it seems likely that variation in gene dosage of key components due to functional regulatory polymorphisms could play an important role in cancer development. Here we provide evidence of the involvement of promoter single-nucleotide polymorphisms (pSNPs) in the cyclin-dependent-kinase inhibitor genes CDKN2A, CDKN2B, CDKN1A, and CDKN1B in the etiology of childhood pre-B acute lymphoblastic leukemia (ALL). A case-control study, conducted in 240 patients with pre-B ALL and 277 healthy controls, combined with a family-based analysis using 135 parental trios, all of French-Canadian origin, were used to evaluate single-site genotypic as well as multilocus haplotypic associations for a total of 10 pSNPs. Using both study designs, we showed evidence of association between variants CDKN2A -222A, CDKN2B -593A, and CDKN1B -1608A, and an increased risk of ALL. These findings suggest that variable expression levels of cell-cycle inhibitor genes CDKN2A, CDKN2B, and CDKN1B due to regulatory polymorphisms could indeed influence the risk of childhood pre-B ALL and contribute to carcinogenesis.

journal_name

Blood

journal_title

Blood

authors

Healy J,Bélanger H,Beaulieu P,Larivière M,Labuda D,Sinnett D

doi

10.1182/blood-2006-02-003236

subject

Has Abstract

pub_date

2007-01-15 00:00:00

pages

683-92

issue

2

eissn

0006-4971

issn

1528-0020

pii

blood-2006-02-003236

journal_volume

109

pub_type

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