A single protein building block commonly found in food may hold a key to preventing the spread of an often-deadly type of breast cancer (Nature 2018; doi:10.1038/nature25465).
Investigators found that by limiting the amino acid asparagine in lab mice with triple-negative breast cancer (TNBC), they could dramatically reduce the ability of the cancer to travel to distant sites in the body. Among other techniques, the team used dietary restrictions to limit asparagine.
Foods rich in asparagine include dairy, whey, beef, poultry, eggs, fish, seafood, asparagus, potatoes, legumes, nuts, seeds, soy, and whole grains. Foods low in asparagine include most fruits and vegetables.
“Our study adds to a growing body of evidence that suggests diet can influence the course of the disease,” said Simon Knott, PhD, Associate Director of the Center for Bioinformatics and Functional Genomics at Cedars-Sinai and a first author of the study.
If further research confirms the findings in human cells, limiting the amount of asparagine cancer patients ingest could be a potential strategy to augment existing therapies and prevent the spread of breast cancer, Knott added.
Research from past studies have found that most tumor cells remain in the primary breast site, but a subset of cells leaves the breast and enters the bloodstream. Those cells colonize in the lungs, brain, and liver where they proliferate.
The researchers discovered that the appearance of asparagine synthetase—the enzyme cells used to make asparagine—in a primary tumor was strongly associated with later cancer spread. In addition, metastasis was greatly limited by reducing asparagine synthetase, treatment with the chemotherapy drug L-asparaginase, or dietary restriction. When the lab mice were given food rich in asparagine, the cancer cells spread more rapidly.
“The study results are extremely suggestive that changes in diet might impact both how an individual responds to primary therapy and their chances of lethal disease spreading later in life,” said the study's senior author, Gregory J. Hannon, PhD, Professor of Cancer Molecular Biology and Director of the Cancer Research UK Cambridge Institute, University of Cambridge in England.