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Blood cancer drugs may help stop breast cancer cells from spreading, according to a new study.

A new experiment on animals revealed that decitabine, a drug used to treat some blood cancers, switches on the gene coding for the protein kinase D1 (PRKD1) that stops the ability of cancer cells to separate from a tumor and spread to distant organs.  PRKD1, which is expressed in cells of the mammary gland, maintains normal function by preventing cells from morphing into a state where they can dislodge and spread.

"Treatment with low doses of decitabine in an animal model of breast cancer restored PRKD1 expression, reduced tumor size, and blocked metastasis to the lung," the study's senior investigator, Peter Storz, Ph.D., a biochemist and molecular biologist at Mayo Clinic in Florida, said in a news release.

"The outcome of patients with invasive breast cancer is less than optimal despite many attempts to improve treatment, including advanced chemotherapy and hormonal therapy," Storz said. "We hope this study offers a new avenue to prevent breast cancer from becoming aggressive and untreatable."

Researchers found that the drug silenced the gene coding for PRKD1 in all but one subtype of invasive breast cancer called invasive lobular carcinoma.

Researchers also developed a test that can be used to measure the amount of PRKD1 that is silenced in patients' breast tumors.

"Because we found that PRKD1 is increasingly silenced as breast cancer becomes aggressive and spreads, the hope is that this test can be further developed and used to predict which patients are at risk for cancer metastasis, and thus may benefit from decitabine," co-researcher Sahra Borges said in a statement.

Decitabine is a demethylating agent. The drug works by turning on beneficial genes that cancer has silenced in order to grow. Researchers explain that treating genes that are silenced is significantly easier than trying to restore the function of mutate genes.

The findings are published in the journal Breast Cancer Research.