Journal of
Computational Biology and Bioinformatics Research

  • Abbreviation: J. Comput. Biol. Bioinform. Res
  • Language: English
  • ISSN: 2141-2227
  • DOI: 10.5897/JCBBR
  • Start Year: 2009
  • Published Articles: 39

Full Length Research Paper

SNP model to address cytosine trios

Sriram Kannan
Graduate Studies, Molecular Mechanism of Disease, NCMLS, Radboud University, K603, Erasmuslaan17, 6525GE, Nijmegen, Netherlands
Email: [email protected]

  •  Accepted: 27 August 2010
  •  Published: 31 October 2010


DNA methylation maintains allele specific gene expression (Chan et al., 2003) in which miRNA influences allele-specific protein expression and SNPs, found inside miRNA, in turn influences tumor susceptibility (Nicoloso et al., 2010). Further, methylated CpGs have been correlated to APC gene in colorectal cancer (Zhang et al., 2007) and retrotranspositions have also been correlated to APC gene (Miki et al., 1992). Another aspect unrelated to it is Tet1 gene, which has been associated with the conversion of methylcytosine to hydroxymethyl cytosine (Tahiliani et al., 2009). DNA methylation might also have a role in the prevention of normal differentiation in pediatric cancers (Diede et al., 2009). As the difference between a nucleobase and its methylated form is its structure and its molecular weight, this research article is focussed on using the molar mass of nucleobases to find out if there is any uniqueness as for the position of occurrence of a nucleotide in a given model. SNPs occurrence position was used as a model in this research for addressing the cytosine trios (cytosine, 5methyl cytosine, hydroxy methyl cytosine) based on molar mass of the nucleobase. As the conditions for occurrence of SNP, at a given position in a sequence, were found to uniformly conform with all 140,000 SNPs analysed, including all clinically associated SNPs from NCBI SNP database, it intrigued conformity to be cross checked with SNPs near experimentally proven methylation sites.


Key words: SNP, molar mass, Tet1, colorectal cancer, methylation.