The University of Hong Kong announced Tuesday a study result about the unravel of a new mechanism for the development of a virus-led leukemia, which provides future direction for exploiting new anti-cancer therapeutic agents.

The research team has identified and characterized for the first time a novel protein in human cells called TAX1BP2 functions to prevent the cell centrosome from duplicating more than once when a cell divides.

It further demonstrated that when HTLV-1 virus, which can cause adult T-cell leukemia (ATL), binds and inhibits protein TAX1BP2, can lead to abnormal numbers of chromosomes, which promote the development of cancer.

The findings, which have been published in a leading international scientific journal Nature Cell Biology on June 11, 2006, have important implications in the rational design and development of anti-cancer therapeutic agents targeted to specific proteins in cancer cells.

The study suggests a new mechanism for retroviral oncogenesis, which is likely shared by other tumor viruses.

Viral infection is a major risk factor for the development of cancer. It was estimated that about 15 percent of all human cancers are attributable to virus infection, including liver and nasopharyngeal carcinoma.

Source: Xinhua