One defining characteristic of cancers is their ability to evade cell death through the elongation of DNA structures called telomeres. The majority of cancers (85%) do this by exploiting the stem cell enzyme telomerase, however a subset (15%) use an alternative method called the alternative lengthening of telomeres (ALT). Telomerase cancers are difficult to target without also targetting useful stem cells, however ALT seems to be entirely distinct from normal cellular processes. Therefore, it appears to be a valuable target for therapy.
My research focuses on the way DNA repair pathways are chosen at the sites of double strand telomere breaks (tDSBs), particularly in ALT cancers. Effective repair of tDSBs is crucial, and can occur by a number of different mechanisms. However, knowing how ALT cancer telomere repair is initiated, and how the cell decides to switch from normal tDSB repair may prove invaluable for creating a targetted therapy.
My work involves the use of commercial cancer cell lines paired with standard molecular biology techniques such as immunohostchemistry and microscopy, ALT specific assays, and also next generation sequencing to attempt to elucidate how tDSB repair is controlled.