Oncogenesis and Aging by Isotopic Functionalizations of the Proteins and Nucleic Acids

Although the dynamics of telomeres during the life expectancy of normal cells have been extensively studied, there are still some unresolved issues regarding this research field. For example, the conditions required for telomere shortening leading to malignant transformations are not fully understood. In this work, we mass analyzed DNA of normal and cancer cells for comparing telomere isotopic compositions of white blood cells and cancer cells. We have found that the 1327 Da and 1672 Da characteristic telomere mass to charges cause differential mass distributions of about 1 Da for determining isotopic variations among normal cells relative to cancer cells. These isotopic differences are consistent with a prior theory that replacing primordial, common isotopes of 1H, 12C, 14N, 16O, 24Mg, 31P and/or 32S by nonprimordial, uncommon isotopes of 2D, 13C, 15N, 17O, 25Mg and/or 33S leads to altered enzymatic dynamics for modulating DNA and telomere codons towards transforming normal cells to cancer cells. The prior theory and current data are consistent also with a recently observed non-uniform methylation in DNA of cancer cells relative to more uniform methylation in DNA of normal cells. We observe further evidence of nonprimordial isotopic accelerations of acetylations, methylations, hydroxylations and aminations of nucleosides with alterations of phosphorylations of nucleotides for possibly explaining the induced mutations of DNA, RNA and proteins leading to cancer and more general alterations of DNA associated with aging. The different mass spectra of normal and cancer DNA may be reasoned by different functionalizations and isotopic enrichments as causing different motionally induced atomic and nucleotide orders by different nuclear magnetic moments (NMMs); many motionally induced oligonucleotides causing nanoscale disorder and chaos; and the many such motionally induced nanoscale chaoses of different genes causing order in macroscopic DNA for organelles organizations.Competing Interest StatementThe authors have declared no competing interest.View Full Text