Biomarin Medical Symposium VO
Description
Vocal Characteristics
Language
EnglishVoice Age
Middle Aged (35-54)Accents
British (General)Transcript
Note: Transcripts are generated using speech recognition software and may contain errors.
DNA is continually subjected to damage that needs to be repaired for cells to survive and replicate. Because cancer cells are rapidly growing and dividing, they rely even more on DNA repair involving the two pathways with functional Bracha and pop. Pop recognises and binds to the damaged DNA and then signals repair proteins to form a complex to fix the DNA. Once the repair complexes formed, Part releases the DNA allowing repair. Functional breaker is also a critical component of DNA damage repair that complements the park mediated pathway. However, when Bracha is mutated in cancer cells, DNA damage repair is compromised and sells rely more heavily on other repair pathways for survival, particularly the pop pathway. Pop can be exploited therapeutically by two distinct mechanisms to prevent DNA damage repair and induce cell death in Bracha mutated tumours. First inhibition of pop prevented from repairing the damaged DNA. Second trapping inhibited pop on DNA forms a complex that blocks access to the damaged DNA by alternative repair pathways in pre clinical models. Forming the pop DNA complex is more likely to induce cancer cell death than inhibition of pop alone. Pre clinical data have demonstrated that utilising two distinct mechanisms is a novel and potent approach to induce cell death in Bracha mutated tumours. First inhibition of POB prevents it from repairing the damage. DNA and second trapping pop on DNA blocks access to the damaged DNA by alternative repair pathways.