Hello Beata, There is a tumor specific mechanism to extent eroded telomeres, called ALT (for alternative lengthening of telomeres). It is telomerase independent, but exploits homologous recombination (requires among many other proteins PML1).

I could imagine that at the pericentromeric regions of chromosomes, short telomeric repeat sequences are there, virtually a rudimentory structure from the pre-Robertsonian fusion of originally acrocentric chromosomes to the present metacentric ones.  Could be that if there are double strand breaks induced in those interstitial telomeric repeats, than the cell exploits ALT to repair them.   But I can not imagine that this is a high fidelity process.

Michael

Have you checked if your cells following DNA damage induction have telomerase activity? 

Thank you for your answer!

Is it a very interesting idea, that ALT mechanisms play a role in double strand repeat! Thanks Michael! I will check the sequence whether  telomere repeats are there at this part of the chromosomes.

And to answer Andrew, I checked the telomerase expression level by WB, but not the activity and I found a considerable higher level of  telomerase compare to normal cells.

Beata

A word of caution, the TERT antibody is not actually detecting hTERT in whole cell lysates, you must puriy telomerase first to remove abundant protein contaminants. It detects a much more abundant protein called nucleolin when whole cell protein lysates are tested using western blots. See the following paper: http://nar.oxfordjournals.org/content/early/2014/07/02/nar.gku560.full

Thus if you truly want an answer to you DSB and telomerase questions you must perform a TRAP assay for telomerase activity or a primer extension assay (TRAP is much easier, the primer extension assay requires large numbers of cells, radioactivity and a special purification procedure that most labs do not have expertise in). I hope this helps.