The research uncovers the likely reason why certain chemotherapies are effective for many patients. Importantly, they also shed light on why endeavors to discover new chemotherapy drugs based solely on stopping cellular division have been so disappointing.indicates that chemotherapy may not be reaching its full potential, in part because researchers and doctors have long misunderstood how some of the most common cancer drugs actually ward off tumors.
“This was sort of mind-blowing,” Weaver says about the previous research. “For decades, we all thought that the way paclitaxel works in patient tumors is by arresting them in mitosis. This is what I was taught as a graduate student. We all ‘knew’ this. In cells in a dish, labs all over the world have shown this. The problem was we were all using it at concentrations higher than those that actually get into the tumor.
“There’s still a lot of the scientific community that’s investigating mitotic arrest as a mechanism to kill tumors,” Weaver says. “We wanted to know — does that matter for patients?” Normally, a cell’s chromosomes are duplicated before the two identical sets migrate to opposite ends of the cell mitosis in a process called chromosomal segregation. One set of chromosomes is sorted into each of two new cells.