Similar gene nutrient interactions have been reported with other polymorphisms in folate metabolism genes, in particular the MTHFR C677T variant (Ma et al, 1997), and it is entirely plausible that the risks conferred by low penetrance colorectal susceptibility alleles may be influenced by environmental exposures that impact on the same metabolic pathways.
With regard to the variation in human pain phenotypes, associations have been reported with single nucleotide polymorphisms (SNPs) in genes coding for catechol-O-methyltransferase (COMT), opioid receptors (OPRM1, OPRD1), transient receptor potential (TRPV1, TRPA1), fatty acid amide hydrolase (FAAH) and α-subunit of voltage gated sodium channel (SCN9A)[ 6- 11].
It has recently been reported that mitochondrial polymorphisms associated with alterations in mitochondrial function play a role in women's risk for invasive breast cancer [ 2] suggesting a role for reactive oxygen species (ROS) production.
Previously, paternal IHD has been reported for offspring with polymorphism in angiotensin converting enzyme (ACE) [ 13].
This finding may explain why functional variation with VDR polymorphisms has been reported insubjects with marked deficiency.
Few results have been reported that associate ER polymorphisms with a change in BMD in women treated with SERMs (Yoneda et al, 2002; Heilberg et al, 2005).
The T337G Tyr113His and A415G His139Arg polymorphisms have been reported associated with 40% decreased and 25% increased enzyme activity [ 14].
The variant of this SNP is associated with an impairment of DNA glycosylase activity [ 18]. hOGG1 Ser326Cys polymorphism has been reported associated with various types of malignancy including lung, esophageal, bladder, and prostate cancer [ 19– 219.
It has been reported that the GSTP1-A105G polymorphism was associated with prognosis of gastric and colorectal cancer patients receiving platinum-based chemotherapy (the mutant 105 G/G homozygous involving with survival benefits [ 11, 49], while wild type 105 A/A homozygous associated with unfavorable clinical outcomes [ 14]).
So far, no other QCA data have been reported in relation with the Pro12Ala polymorphism.
