healthmedicinet

New research conducted by Harvard scientists is laying out a roadmap to one of the holy grails of modern medicine – a cure for cancer.

As described paper recently published in eLife, Nowak, a professor of Mathematics and of Biology and director of the Program for Evolutionary Dynamics, and co-author Ivana Bozic, a postdoctoral fellow in mathematics, show that, under certain conditions, using two drugs in a “targeted therapy” – a treatment approach designed to interrupt cancer’s ability to grow and spread – nearly all cancers could be effectively cured.

Though not a cure for cancer, Nowak said the research does offer hope to researchers and patients alike by demonstrating that it may soon – possibly sooner than many might think – be beaten.

“In some sense this is like the mathematics that allows us to calculate how to send a rocket to the moon, but it doesn’t tell you how to build a rocket that goes to the moon,” Nowak said. “What we found is that if you have a single point mutation in the genome that can give rise to resistance to both drugs at the same time, the game is over. We need to have combinations such that there is zero overlap between the drugs.”

Importantly, Nowak said, for the two-drug combination to work, both drugs must be given together – an idea that runs counter to the way many clinicians treat cancer today.

“We actually have to work against the status quo somewhat,” he said. “But we can show in our model that if you don’t give the drugs simultaneously, it guarantees treatment failure.”

In earlier studies, Nowak and colleagues showed the importance of using multiple drugs. Though temporarily effective, single-drug targeted therapy will always fail, they showed, because the disease eventually develops resistance to the treatment.

To determine if a two-drug combination would work, Nowak and Bozic turned to an expansive data set on how patients respond to single-drug therapy, supplied by clinicians at Memorial Sloan Kettering, to create computer models of how multi-drug treatments would work. Using that model, they then treated a series of “virtual patients,” creating using data, collected by another contributor, on the number of cancer cells that had colonized recently-deceased patients.

“For a single-drug therapy, we know there are between 10 and 100 places in the genome that, if mutated, can give rise to resistance,” Nowak explained. “So the first parameter we use when we make our calculations is that the first drug can be defeated by those possible mutations. The second drug can also be defeated by 10 to 100 mutations.