Thesis

General introduction and thesis outline 21 1 cancer by considerably deregulating tumour suppressor genes and oncogenes. Cellular, or so-called host-cell, DNA methylation markers have been recognised as sensitive biomarkers for transforming CIN lesions 25. Early lesions are characterised by low levels of DNA methylation, while advanced lesions with a high cancer progression risk are characterised by high/increased levels of DNA methylation. 1.3 CERVICAL CANCER PREVENTION Cervical cancer is highly preventable and treatable if detected early and managed effectively. Despite this, it remains a leading cause of cancer-related deaths among women worldwide. To combat cervical cancer, the World Health Organisation (WHO) CH3 Unmethylated Promoter region Promoter region Cytosine DNMTs 5-Methylcytosine Methylated Unmethylated Methylated Tumour suppressor gene Tumour suppressor gene CH3 CH3 CH3 CH3 CH3 CH3 Figure 1.6 DNA methylation-mediated silencing of tumour suppressor genes. DNA methylation is an epigenetic process that controls gene expression and plays a significant role in the development of cervical cancer. The process of DNA methylation is regulated by DNA methyltransferases (DNMTs), which binds a methyl (-CH3) group to the carbon-5 position of a cytosine molecule in CpG dinucleotides. This process generally leads to the repression of gene transcription, particularly in promoter regions of tumour suppressor genes that have a high density of CpG sites and is commonly observed in cancer cells. Abbreviations: DNMTs, DNA methyltransferases; CH3, methyl group; C, cytosine; Me, methylation

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