A cancer-fighting gene known as the “guardian of the genome” actually promotes certain tumors, according to a study by researchers at the University of California, San Diego. That means drugs that affect its activity may backfire in some cases, fueling a tumor’s growth.

The gene, called p53, makes a protein that causes abnormal cells to self-destruct before they turn malignant. Mutated forms of the gene don’t perform this function as well.

About half of cancers have a mutated p53 gene, making it the most commonly mutated gene in malignancies. As such, it has been a major target of drug development to restore normal function. But in certain instances restoring normal function could help the tumor grow. So knowing what these drugs will do to a particular cancer is vital.

The study demonstrates a point that oncologists have been making for decades: Cancer is not one disease. What we call cancer is hundreds of genetic diseases that share certain characteristics. And as knowledge grows about the differences between cancers, the desirability of personalized treatment becomes more evident.

Researchers led by Yang Xu based their results on studies of human patients, cell samples and mouse models of cancer. The study

Cancers often occur gradually, with a series of mutations that weaken genetic defenses against abnormal growth. Their degree of aggressiveness also varies. Some cancers are rapid-growing and require immediate treatment. Other cancers are slow-growing, and may not need immediate treatment.

Slow-growing cancers can cross a threshold and begin to spread rapidly. The activity of p53, or the lack of it, helps determine if and when that threshold is reached.

Ovarian cancer is one example in which the lack of normal p53 is implicated. In some aggressive ovarian cancers, the gene is mutated nearly all the time. But the gene is much less frequently mutated in hepatocellular or liver cancers.

Xu and colleagues found that restoring p53 function in mutated liver cancer cells improves their metabolism by indirectly causing cells to switch to a process called glycolysis, which involves the heavy use of sugar as an energy source.

Normally, cells use a process that is more energy-efficient but limited by the availability of oxygen. Called oxidative phosphorylation, it takes place in mitochondria, organelles in cells that provide most of the body’s energy.

This metabolic change to glycolysis, called the Warburg effect, has been recognized for decades as a characteristic of cancer.

So in liver cancers, promoting p53 function will induce this metabolic shift, energizing the cancer.

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