Washington D.C. [USA], Dec. 31 : A team of US researchers suggested a new mechanism that controls blood cell function and several possible molecular targets for treating blood cancer.
The researchers found that over expression of a protein, called TRAF6 , in blood cells drives the onset of myelodysplasia syndromes (MDS) - a group of pre-malignant disorders in which bone marrow does not produce enough healthy blood cells.
According to the authors, TRAF6 normally functions as an immune sensor of pathogens and MDS can lead to acute myeloid leukemia (AML), a fast-spreading blood cancer that can be deadly if not treated promptly.
The study was published in the journal of Nature Immunology.
"We found that TRAF6 over-expression in mouse hematopoietic (blood) stem cells results in impaired blood cell formation and bone marrow failure," said lead study author Daniel Starczynowski from Cincinnati Children's Hospital Medical Center.
"Based on our paper, a number of therapeutic approaches can be tested and directed against TRAF6 and other related proteins responsible for MDS," Starczynowski added.
They also found molecular interactions with Cdc42 - a protein that helps regulate cells also implicated in cancer.
All of these could be potential treatment targets for cases of MDS triggered by over-expression of TRAF6, Starczynowski explained.
The researchers were able to identify the new molecular targets by conducting a global proteomic analysis of human leukemia cells. This allowed them to the see entire complement of proteins regulated by TRAF6 in leukemia cells.
Beyond the potential for new therapeutic approaches in treating MDS or AML, the paper revealed a new and critical immune-related function for TRAF6, according to the authors.
In response to various pathogens, the protein also regulates RNA isoform expression, an important step in the translation of genetic code into protein and cell formation.