Seminars

   The transcription factor c-MYC is often deregulated in cancer cells. It promotes DNA replication and increases histone H2AX phosphorylation, a hallmark of DNA double-strand breaks, suggesting that c-MYC induces genomic instability during tumorigenesis. Paradoxically, it is well known that oncogenic c-MYC protects cancer cells from devastating DNA damage. Apparently, there are two opposing roles of c-MYC in DNA damage response. Because the abundances of oncogenic c-MYC in chemosensitive cancer cells and chemoresistant cancer cells are similar to one another, we hypothesize that there is a c-MYC co-factor, through which c-MYC shifts its function in genomic instability. Therefore, the learning objectives of this seminar will be:
1)To identify a possible c-MYC co-factor that modifies the sensitivity of cancer cells to DNA damage, and
2) To determine how c-MYC increases the resistance of cancer cells to DNA damage.Cancer chemotherapy using conventional DNA-damaging compounds, such as cisplatin, is one of the main-line therapies used daily and routinely for many cancer patients. However, cancers eventually acquire chemoresistance, which, in many cases, causes treatment failure. Our study will determine how cancer cells become resistant to DNA damage, and how we can re-sensitize chemoresistant cancer cells to DNA-damaging therapeutic agents.