Why Genetic Medicine Is Tricky

So there's a great deal of enthusiasm here and elsewhere - such as this swell DNA Network I'm a part of - for the power of genetic based medicine. The overarching idea is temptingly simple: Once we can spot the genes that cause disease (whether individually or in combination) we'll be able to intervene earlier and treat better. On paper, it's a pretty plain proposition. All we have to do is map out the range of genetic traits and preconditions, and we'll be able to maximinze the good genes and minimize the bad ones (this is, of course, a gross simplification). But:

Turns out this is harder in practice than in principle. Consider this recent news about a discovery at the Georgia Institute of Technology that turned upside-down a commonly held perception of one particular gene. Published in Plos One, the gist is that a gene scientists thought helped chemotherapy destroy cancer cells actually may, in fact, help cancer thrive. Here's the lowdown:

When a cell is malfunctioning or injured, the gene p53 is called into action and tries to repair the cell. If the cell can't be repaired, p53 starts a process known as apoptosis that kills the cell. It's p53's role as one of the genes involved in initiating cell death that has led cancer researchers to long believe that the gene is essential to successful chemotherapy. The idea is that p53 assists in killing the cancerous cells that the chemo treatment injures.

But in this latest trial, Georgia Tech researchers found that p53 may be a "double-edged sword." Chemotherapy patients whose tumors had a mutated p53 gene that didn't work had a much better survival rate than those who had normal p53.

So here's my take-away: We may be moving forward fast on mapping out the varieties of the human genome. And we may be quickly learning which genes do what and why. But genes are very tricky things. They don't act, as they're often described, like computer code - that is, in a binary either/or way. Rather they have multiple characteristics with multiple effects. The idea that we can simply turn certain genes on - to improve good effects - and turn other genes off - to reduce ill - is a superficial, and ultimately naive approach. In other words, it's going to take much longer to work all these characteristics out than is commonly described.