SINGAPORE - Tumour growth can be slowed or prevented by "starving" cancer cells of a nutrient commonly found in meat, fish and dairy products, a local study has found.
Researchers from the Agency for Science, Technology and Research (A*Star) and the National Cancer Centre Singapore (NCCS) discovered that cancer stem cells use an amino acid called methionine as fuel and are especially dependent on it.
Cancer stem cells are responsible for tumour growth and repair, but the bulk of a tumour is made up of non-stem cancer cells, said Dr Daniel Tan, 41, a senior consultant at the division of medical oncology at NCCS and a member of the research team.
The team found that starving lung cancer cells of methionine for 48 hours resulted in a "dramatic" 94 per cent reduction in tumour size compared with a control sample, he said.
Starving the cells of other amino acids like glutamine, glycine and serine, which are used by non-stem cancer cells, was found to have only mild effects on reducing the tumour size .
Drug resistance is a persistent problem for cancer treatment research, Dr Tan said.
Conventional cancer treatments like chemotherapy are effective in targeting non-stem cancer cells but leave behind cancer stem cells, he added.
This leads to the cancer becoming resistant to the chemotherapy drug over time as the cancer stem cells regenerate the other types of cells.
"We are hoping that this approach of targeting the nutrient dependency of cancer stem cells can offer another way of treating lung cancer and other solid tumours," said Dr Tan, adding that the study found a similar dependency in breast cancer, ovarian cancer and leukaemic cells.
However, methionine is an essential amino acid that is also used by healthy tissue and it is not feasible to remove it completely from one's diet, said Dr Tam Wai Leong, 41, group leader for precision oncology at the Genome Institute of Singapore under A*Star.
Dr Tam, who is also the study's senior author, said: "What we can do is to prevent the cells from using methionine by inhibiting an enzyme called MAT2A, which converts the methionine into a compound that is involved in critical gene functions in cancer stem cells."
A drug that inhibits MAT2A is not currently available on the market, but the team is working on developing one for clinical trials, he said.
He added that biotechnology companies in the United States are also conducting early trials on a similar drug to disrupt the methionine metabolic cycle in various other types of cancer.
But it will be important for clinicians to select the patients who are most likely to benefit from such a drug, Dr Tam said, as it may not be effective in tumours that express low or no levels of MAT2A.
The study was funded by A*Star and the National Medical Research Council.