Carcinoma development includes tumour suppressor gene inactivation and proto-oncogene activation which provide the tumour with malignant characteristics such as unlimited and unregulated cell growth and division, ability to invade surrounding tissues and form mestastasis as well as to induce angiogenesis. Epigenetic mechanisms in carcinogenesis are equally important as mutations in DNA. In homeostasis there is a balance between DNA methylation and demethylation within a cell, while in tumour cells global hypomethilation and local hypermethyilation have been observed. Local hypermethyilation most commonly affects promoter regions and is associated with gene inactivation while global hypomethilation contributes to chromosomal instability as it is associated with chromosomal rearangements which lead to aneuplody, translocations and deletions. Moreover, 5-methylcytosine increases the rate of point mutations for spontaneous deamination and causes cytosine to tymine transversions. Both methylation driven gene inactivation and demethylation of silenced genes represent risk for tumour development. The role of p16-INK4a, p14ARF, p53, pVHL proteins and heparanase illustrate the complexity of cellular processes whose dysregulation leads to tumorigenesis and affect the malignancy. The aim of this work was to show the characteristics of DNA methylation and consequential effects on the genome, as well as to emphasize the importance of DNA methylation in carcinogenesis. Using known examples of DNA methylation changes in carcinoma, the aim was to show its potential as diagnostic and prognostic marker.