ANDRZEJ KRAUZEIn the early 2000s, scientists were first starting to appreciate the idea that microRNAs—small, noncoding RNAs that interfere with protein translation—could have something to do with cancer. One clue came from developmental biology, when Frank Slack, then at Yale University, and colleagues found that mutating a microRNA gene called let-7 led to increased cell divisions. Then in 2002, Carlo Croce’s team, then at Thomas Jefferson University in Philadelphia, mapped genetic deletions common in chronic lymphocytic leukemia to two microRNA loci, miR15 and miR16.
Now, a little more than a decade later, “we know that microRNA levels are essentially abnormal in every type of tumor that’s been examined,” says Joshua Mendell, a microRNA researcher at UT Southwestern Medical Center. In some tumors, a microRNA may be overexpressed, while in others it may be missing altogether.
Some experimental studies have also shown that manipulating a microRNA associated with a cancer—say, deleting one that’s overexpressed or boosting one that’s in low abundance—can knock back tumors. Such is the case with miR15 and miR16, for instance. After Croce and colleagues found that these genetic loci are missing or downregulated in more than half of B-cell chronic lymphocytic leukemias (CLL), another group demonstrated that experimentally deleting this region in mice causes symptoms similar ...
