Cancer research has discovered that when double-strand break DNA damage occurs, in which both strands of the DNA double helix are severed, the cell can either attempt to repair the damage, which has a poor chance of success and may create a cancerous cell (or a more aggressive clone of an existing cancerous cell), or it can trigger its own death (apoptosis). Further research has found how we can possibly drive cells toward apoptosis rather than the gluing repair method when a double break occurs. This opens up the possibility of developing a drug for use when treating a patient with chemotherapy. The drug would reduce the chances of more aggressive cancerous clones arising from attempted repair of chemo damaged DNA; the cells with double strand breaks would be more likely to take the apoptosis path:
"What we propose is increasing the level of 53BP1 to force cancer cells into the error-prone pathway where they will die," says Youwei Zhang, assistant professor of pharmacology at the Case Western Reserve University's School of Medicine. "The idea is to suppress deliberately the second accurate repair pathway where cancer cells would prefer to go. It is a strategy that would lead to enhanced effectiveness of cancer therapy drugs.”
Getting to this point has required decades of work; a comment to the Gizmag article references a paper identifying the function of this 53BP1 binding protein in mice over 10 years ago.
Wouldn't it be great if the billions spent on cancer research, so despised by Richard Smith of the cancer the best way to die infamy, did turn up a treatment helper drug with wide application across a range of different cancer types?