Notably, the altered genomic regions encompass, which harbours the DNMT1 gene, which plays a role in the establishment and regulation of tissue-specific patterns of methylated cytosine residues. The DNA CN alterations of DNMT1 in advanced stages primary melanomas raise crucial questions: Is demethylation, contributing to clinical outcomes, only a passive consequence of CN loss? Or do CN alterations – as was demonstrated in the context of epigenetic mechanisms and the BRAFV600E mutation – directly control the DNA methylation changes to influence the gene expression patterns of given molecules? Regardless of the reason for changes in methylation, we obtained better insight into how gene expression levels are regulated by DNA methylation: demethylation was associated with increased mRNA levels, whereas hypermethylation was associated with decreased levels. In summary, we demonstrated the strong influence of DNA methylation changes on melanoma progression. However, hypermethylation, which has been greatly emphasised in the literature, appears to represent more complexity both in melanoma initiation and progression. Additionally, the inhibition of promoter hypermethylation might represent the most promising therapeutic target for the treatment of melanoma, and several types of DNMT inhibitors are currently being developed. Considering the dual role of DNA methylation, further efforts are needed to investigate the importance of such drugs in melanoma treatment. Approximately 225,000 new cases of ovarian cancer were diagnosed in 2008 worldwide, comprising 4% of all female cancers. The majority of ovarian cancers are epithelial, frequently present at advanced stages and are associated with high mortality rates. Therefore, investigating the function and expression of potential prognostic proteins is essential for the advancement of our understanding of the molecular pathogenesis of epithelial ovarian cancer. This is especially desirable with regards to the identification of diagnostic biomarkers for patient management. The MCPH1 and MCPH5 genes encode Microcephalin and the abnormal spindle-like microcephaly-associated protein respectively. MCPH1 and MCPH5 are two of ten microcephaly genes identified, which are implicated in autosomal recessive primary microcephaly. Microcephaly is characterized by reduced foetal brain growth resulting from mitotic defects during embryonic brain development. Microcephalin is a nuclear and cytoplasmic protein consisting of 835 amino acids. The protein contains three BRCA1 C-terminus domains, one N-terminally located and two in the Cterminus. Microcephalin is involved in DNA damage response with a further role as a regulator of chromosome condensation preventing cells from entering mitosis before DNA replication is completed. Microcephalin is also known as BRIT1, which was initially identified as a transcriptional repressor of human telomerase reverse transcriptase, the catalytic subunit of human telomerase.