Unlimited proliferative capacity of tumor cells and immortal cell lines depends on their ability to maintain their telomeres, usually by activating telomerase, an RNA-dependent DNA polymerase that adds telomere repeats directly on the ends of chromosomes by reverse-transcribing an endogenous RNA template. On the other side, a number of tumors can also lengthen their telomeres without telomerase by means of alternative lengthening of telomeres (ALT). ALT is based on recombination-dependent replication processes that can use other telomeres or extrachromosomal telomeric repeats as templates for telomere elongation. Molecular basis of these processes are not yet clear. ALT activity has only been detected in abnormal cells and it seems that it is closely related to dysfunction in telomeres. These telomere dysfunctions compromise the roles they normally play in chromosome end protection and chromosomal ends are recognized as double stranded breaks caused by DNA damage. The telomere elongation itself is, by that definition, a consequence of cell repair machinery constantly acting on telomeric DNA. Telomere maintenance mechanisms could be used as a good target for cancer treatment because they appear in all tumors but not in healthy cells, so their inhibition should show minimal side-effects. Most research in that direction is based on telomerase inhibitors but for most successful results ALT also needs to be taken in consideration and its mechanisms and genetic background further investigated.