Although the dynamics of telomeres during the life expectancy of normal cells has 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 among normal cells relative to cancer cells. These isotopic differences are consistent with a prior theory according to which 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. This replacement may subsequently modulate DNA and telomere codons resulting in transformation of normal cells to cancer cells (in 15 N depletion in telomeres dependent manner). The prior theory and the current data are consistent also with a recently observed non-uniform methylation pattern of the DNA of cancer cells relative to a more uniform methylation in the 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; which may explain the induction of mutations at the DNA, RNA and proteins leading to cancer and more general alterations of DNA, which are associated with aging. This difference in mass spectra between normal and cancer DNA may stem from different functionalizations and isotopic enrichments affecting the motion derived from nuclear magnetic moments (NMMs). We suggest that this phenomenon may lead to malignant transformation.
© 2023 The Authors. Published by Elsevier Ltd.