Scientists in Hong Kong believe they have uncovered the trigger for leukemia, a cancer of the blood that afflicts millions worldwide.

The findings could pave the way for the design of new drugs to combat the abnormal proliferation of white blood cells and might also lead to new treatments for other types of cancers.

Leukemia has been linked to infection by the Human T-cell Leukemia Virus type 1 (HTLV-1), which is contracted through sex, blood transfusions and breastfeeding.

More than 20 million people suffer from leukemia globally and it is especially prevalent in Japan.

In a study that began in 2000, researchers at the University of Hong Kong found that abnormal division of white blood cells took place when a foreign protein called TAX in the leukemia virus bound itself to a human protein which the same group of scientists identified for the first time in human cells.

That newly identified protein, called TAX1BP2, ensures proper cell division.

When the foreign protein started merging with the human protein, the scientists began to observe abnormal cell division.

“When they merge, the function of TAX1BP2 is disrupted ... and leads to the generation of abnormal numbers of chromosomes in daughter cells and is therefore thought to be a driving force in the development of cancer,” said Wilson Ching, assistant professor of the University of Hong Kong’s departments of pathology and biochemistry.

The group’s findings were published in the journal Nature Cell Biology on June 11.

The researchers will see if their findings apply to other types of virus-linked cancers, such as liver cancer, which is believed to be linked to the hepatitis B virus, and nasopharyngeal cancer, linked to the Epstein-Barr virus.

The latter two cancers are endemic in southern China and Hong Kong. Up to 10 percent of Hong Kong’s population were estimated to be carriers of hepatitis B just five years ago.

At least 15 percent of all human cancers are believed to be caused by viral infections.

The team’s findings might also help pave the way for the design of new drugs to stop the foreign protein from disrupting normal cell division.

“We’re thinking of a way to block or inhibit the binding of TAX to the human protein. If you can block this binding, then, it will stop this foreign protein from causing cancer,” Ching said.