The aim of this PhD thesis was to investigate the DNA methylation pattern and influence of DNA demethylating agent 5-azacitydine (5azaC) on the development of experimental mouse teratocarcinoma (TCa) obtained by the transplantation of gastrulating mouse embryo (E 7,5) under the kidney capsule of an adult animal. It was discovered that TCa develops from male embryos only. Investigated 8- week long period of TCa development started with subtle growth followed by resting phase. TCa development ended with explosive growth paralleled with concomitant increase in expression of Pcna gene (proliferation marker). In vitro experiments have pinpointed the key role of stemness genes Oct3/4 and Nanog expression since their esiRNA induced inhibition caused the suppression of tumour development from the embryo. Through analysis of DNA methylation pattern we discovered continuing hypomethylation of Nanog gene during TCa development compared with normal testicular tissue. Contrary, compared with embryo development, Oct3/4 gene showed hypermethylation reprogramming overlapping with the period of tumour subtle growth and resting phase period. Achieving the maximum hypermethylation phase, TCa initiated the intensive growth correlating with proportion of Oct3/4 demethylated cells. Sox2 gene, although with low percentage of DNA methylation, showed the promoter methylation reprogramming during TCa development similar to the one established for Oct3/4 gene promoter. Based on the promoter DNA methylation pattern analysis of Scgb3a1, Prss21, Stat3, Brca1, Mgmt, c-Myc, Trrap and Rassf1 genes and established global methylation pattern based on the analysis of Mml, Mmetnltr and B1 repetitive DNA sequences it may be concluded that these genes and repetitive sequences are not involved in teratocarcinoma development. 5azaC applied immediately after the embryo transplantation completely inhibited teratocarcinoma development whereas applied on already developed teratocarcinoma, decreased its growth with statistical significance. Despite the fact that 5azaC causes global hypomethylation, its application did not influence the methylation status and reprogramming of stemness genes Oct3/4, Nanog and Sox2. Quite contrary, treatment with 5azaC inhibited the expression of Oct3/4 and Nanog genes in developed teratocarcinoma by some other mechanisms that did not include DNA methylation change. Our results showed that 5azaC treatment does not cause changes of oxidative stress markers nor the markers associated with the inflammation process. According to our obtained results it seems that 5azaC influence the establishment of methyloma which encourages apoptosis and decreases proliferation of TCa stem cells. Our research reveals the epigenetic platform of TCa development and potentials of 5azaC in the treatment of testicular germ cell tumours.