Scientists Find New Way to Attack Cancer's Toughest Target

For decades, cancer researchers have been chasing one of medicine's most wanted targets: a gene so notorious they nicknamed it McGene.

The gene, called MYC, drives aggressive tumor growth in 70% of all cancers. Unlike other cancer genes that get damaged by mutations, MYC is perfectly normal but gets turned up way too loud, acting like a conductor that orchestrates cancer's ability to grow, spread, and hide from the immune system.

The problem? MYC has been considered "undruggable" because it lacks the pockets and grooves that medicines need to latch onto. It's like trying to grab a floppy noodle that constantly changes shape.

Now scientists at Fox Chase Cancer Center in Philadelphia have found a potential workaround. Instead of attacking MYC directly, they discovered two molecular switches that control how many copies of the gene cells produce.

Think of these switches as punctuation marks that change a sentence's meaning, explains Dr. Johnathan Whetstine, who led the study. "Let's eat, grandma" versus "Let's eat grandma" shows how placement matters.

One switch, an enzyme called KDM4C, tells cells to make extra MYC copies. The other, SETD2, keeps MYC in check. When researchers blocked KDM4C with an experimental drug in lab dishes and mice, the number of extra MYC copies dropped.

The discovery, published Friday in Molecular Cell, reveals that extra MYC isn't just random chaos in cancer cells. It's controlled by a specific biological process with a "good guy" enzyme that stops MYC and a "bad guy" that lets it pile up.

This is early science, far from patient treatments. But it represents real progress against a target that's been on cancer research's shortlist alongside KRAS, the mutated gene in most pancreatic cancers.

Why This Inspires

Other research teams are also making headway. A 2024 clinical trial showed some success with a small protein that directly targets MYC. Other labs are going after MYC's partner molecules as an indirect approach.

The big question remains whether blocking something so central to all cells will cause serious side effects. But after decades of MYC seeming impossible to stop, scientists now have multiple promising paths forward.

"I think all roads lead to MYC; however hard you try to ignore it, it's there," says Dr. Marc Mansour, a cancer researcher at University College London not involved in the study.

What once seemed like an unbeatable opponent now looks like a puzzle scientists are finally learning to solve.