With each somatic cell division, the chromosomal ends, or telomeres, progressively short­en. Critically shortened telomeres are recognised by DNA repair systems as DNA damage, the cells are withdrawn from the cell cycle, senesce and eventually die. Mutations in the genes responsible for cell division cycle control, or repression of their protein products, enable cells to continue their proliferation. In the period of the so-called extended life span the cells acquire additional genetic mutations, telomeres progressively shorten, and genomic instability increases. Due to the extremely shortened telomeres accompanied by accumulation of genet­ic abnormalities and increased genomic instability, most cells enter the period of crisis and die. Those cells that can prevent telomere shortening escape crisis and continue to prolif­erate. Due to the stabilised telomeres they have the ability to proliferate indefinitely. The only known mechanism so far by which human cells can regulate the length of telomeres is by the action of the enzyme telomerase. Detection of telomerase activity in the overwhelming majority of advanced and metastatic human cancer but not in most somatic cells implies that telomerase dependent immortalization could contribute to the development of malignan­cy. Thus, repression of telomerase activity may be a novel adjuvant therapy for the treatment of human cancer and detection of telomerase activity may be important for cancer diagnostics. In the present review we have described the most recent advances in the field of telomeres and telomere related proteins, the so-called telomeric complex, its structure and function. Furthermore, we have also outlined the structure, function and mechanisms, by which telom­erase regulates the length of human telomeres. Finally, the current views on the role of telomerase in human cancerogenesis are presented.