Mark L. Gonzalgo

TL;DR: Two major mechanisms by which DNA methylation may lead to aberrant cell cycle control are investigated: through the generation of transition mutations via deamination-driven events resulting in the inactivation of tumor suppressor genes, or by altering levels of gene expression through epigenetic effects at CpG islands.

TL;DR: There is growing evidence that methylation plays a pivotal role in key developmental processes such as genomic imprinting and stabilization of X-chromosome inactivation, and it therefore is not surprising that alterations in this essential epigenetic system might play a role in carcinogenesis.

TL;DR: The data suggest that de novo methylation is not restricted to the S phase of the cell cycle and that transcription through CpG islands does not inhibit theirRemethylation, which occurred most rapidly in the p16, PAX-6, and c-ABL genes, shown to be transcribed prior to drug treatment.

TL;DR: PCR-based techniques can be reliably used for the accurate detection and quantitation of aberrant levels of DNA methylation in tumor specimens, and methylation-associated gene silencing does not represent a common mechanism for p16 inactivation in sporadic melanoma.