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Association between the p21 codon 31 A1 (arg) allele and lung cancer.

In previous investigations p53 polymorphisms and haplotypes have been found to be associated with different types of cancer. In this paper the codon 31 polymorphism of the p53-inducible protein p21 was studied in 144 Swedish lung cancer patients and two different control groups: 95 patients with chronic obstructive pulmonary disease (COPD) and 761 healthy controls. An increased frequency of the p21 codon 31 A1 (arg) allele was found in lung cancer patients, especially in comparison with COPD patients (p = 0.004). There was a significantly increased frequency among lung cancer patients of individuals carrying the arg allele both in comparison with COPD controls (OR = 5.2, 95% CI 1.5-18.1) and healthy controls (OR = 1.7, 95% CI = 1.0-2.9). The results of this and previous studies indicate that allelic variants of both p53 and its effector protein p21 may have an influence on lung cancer.

Alleles↗

PubMedDate not supplied

Effect of p53 alleles on placental weight.

The relationship between three p53 polymorphisms (BstUI and MspI RFLPs in exon 4 and intron 6, respectively, and a 16-bp duplication in intron 3) in placental tissue and placental weight was examined in an attempt to elucidate the effect of p53 alleles on non-malignant growth. Placental tissue is expressing the fetal genotype. Using the quantitative trait loci approach, allelic frequencies of the three p53 polymorphisms and ten alleles at other loci (ABO, PLAP, GC and ACP1) were compared for the high (> or = 700 g) and low (< 400 g) tails (+/- 1.4 SD) of the placental weight distribution in a Swedish sample of newborns. Significant associations were found in the three p53 polymorphisms examined but not for the other loci, suggesting that non-malignant cell growth may be influenced by polymorphic p53 variants. High placental weight was associated with increased frequencies of the 16-bp duplication (A2 allele), the codon 72 BstUI A1 (pro) allele and the MspI A1 allele. These three alleles were in strong linkage disequilibria, and high placental weight was therefore associated with the 2-1-1 haplotype. The fact that the strongest associations were found with intronic markers suggests linkage disequilibrium with growth-promoting sites at the p53 molecule as the most likely mechanism, although a direct functional involvement of the codon 72 pro/arg substitution in normal cell growth cannot be excluded.

Alleles↗