A new international study led by the University of Copenhagen in Denmark has taken a significant step toward the prevention of type 1 diabetes, by showing how low doses of a cancer drug stopped it developing in disease-prone mice.

The treatment also protected the insulin-producing cells in the pancreas from being destroyed.

Dr. Dan Ploug Christensen, of the Department of Biomedical Sciences at the University of Copenhagen, and colleagues, report their findings in a recent online issue of the Proceedings of the National Academy of Sciences.

Type 1 diabetes is classed as an autoimmune disease, where for reasons that are not fully understood, the immune system attacks the insulin-producing beta cells in the islets of Langerhans in the pancreas. The body needs insulin to help regulate blood sugar.

There is currently no cure for the disease, which has to be treated with several insulin injections a day.

The incidence of type 1 diabetes varies widely among differents part of the world, but overall it is rising at around 3% a year. Scientists believe the risk of developing the disease is a combination of genes and environment.

A study presented at a conference in 2013 suggested the global rise in type 1 diabetes may be linked to reduced exposure to infectious diseases in early life.

The new study suggests the cancer drug, which is used to treat lymphoma, works by lowering so-called “sterile inflammation.”

Dr. Christensen says:

Diabetes is a growing problem worldwide. Our research shows that very low doses of anticancer drugs used to treat lymphoma – so-called lysine deacetylase inhibitors – can reset the immune response to not attack the insulin-producing cells.

Our results are a step towards developing a preventive treatment for type 1 diabetes.”

He says when they gave the drug to mice prone to develop type 1 diabetes, they found fewer immune cells in the pancreas, and more insulin was produced.

For the study the researchers used drug doses that are 100 times lower than those used in treating cancer. The lower doses have been shown to be safe in children with certain rheumatic diseases.

The drug works by blocking the molecules that send harmful inflammation signals to the insulin-producing cells in the pancreas, as Dr. Christensen explains:

“In doing so, it prevents the cells from producing a number of factors which contribute to destroying the cells when exposed to inflammation.”

The researchers also showed that the cancer drug delayed the destruction of human cells in donated insulin-producing tissue that was subjected to the inflammation signals.

The next step will be to test the drug in clinical trials to see if it prevents development of type 1 diabetes in people at higher risk for the disease, for instance in those whose close relatives already have it.

Meanwhile, in June 2013, another team in the US revealed how a type 1 diabetes vaccine showed promise in a small trial.

In that study, led by Stanford University School of Medicine, researchers tested a DNA-based vaccine that switches off the part of the immune system that destroys insulin-producing pancreatic cells. The vaccine is unusual in that most vaccines are designed to boost the immune system.