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A new study shows that starving kidney cancer cells can help to kill them off, according to the journal Cancer Research.

Cancer cells are always hungry, as they are constantly altering their metabolism so that they can tap additional fuel to grow and spread.

While Duke University researchers starved the cells of the amino acid cysteine in an experiment, they started a kind of cell death, or necrosis, in mice that carried the illness.

"We found that the same machinery that makes these tumors so aggressive also makes them vulnerable to nutrient deprivation," said senior study author Jen-Tsan Ashley Chi, Ph.D., associate professor of molecular biology and microbiology at Duke University School of Medicine, in a news release. "It is like we are beating it at its own game."

Even as three-fourths of renal cell carcinomas are characterized by a missing VHL tumor-suppressor gene preventing the development of tumors in healthy cells, researchers examined how single genetic changes could change the metabolism and resource needs of the cancer cells.

In a test, scientists took off every one of the 15 amino acids from their growth media. Most of the cells could withstand the change, but with the removal of the cysteine, the cells swelled and floated up, which indicated "neurotic death".

Cystine keeps up the antioxidants, which disarm free radicals of oxygen. But when it is got rid of, the cancer cells died of free radical damage, say, scientists.

Tang's team in Dr. David Hsu's lab at the Duke Cancer Institute put in renal cell carcinoma tumors into mice and treated them with sulfasalazine, blocking cystine uptake.

This helped to spark necrosis and delay tumor growth. Hence, it is important to attack cancers with necrosis, not by apoptosis, in order to lead to cancer therapies.

"Most chemotherapies kill cancer cells through apoptosis, and the cancer cells that escape apoptosis are the root cause of chemotherapy resistance and tumor progression," said Chi. "Cystine starvation treatments could address resistance by killing cells through a different mechanism."