A remedy for the more common form of blood cancer known as multiple myeloma may be on its way amidst reports that researcher in the United States have managed to spot a culprit gene behind the hitherto incurable disease.

Researchers from the department of Genetics and Pathology, Rudbeck Laboratory, Uppsala University have developed a new model that can detect and stop the progression of multiple myeloma. They have spotted the gene after studying a large number of people suffering from multiple myeloma. The researchers also succeeded in “silencing” the genes in the deadly plasma cells via epigenetic mechanisms.

Silencing of a gene effectively means rendering it out of action. “This silencing may lead to the uncontrolled growth of the malignant cells,” says lead author of the study, Dr. Helena Jernberg Wiklund while detailing on the new findings in July edition of the online journal PLoS One.

Further research found the protein called the Polycomb repressor complex (PcG) controls over the silenced genes in the malignant plasma cells. PcG complex has been found to be responsible for self-renewal and distribution of normal embryonic stem cells.

The Uppsala university researchers believe that the PcG complex could possibly help in expansion of the tumour-causing cells of multiple myeloma.

Multiple myeloma is a cancer that begins in plasma cells, a type of white blood cell. These cells are part of the human immune system, which helps protect the body from germs and other harmful substances. In time, myeloma cells collect in the bone marrow and in the solid parts of bone.

In multiple myeloma, the overgrowth of plasma cells in the bone marrow can crowd out the normal blood-forming cells. This can cause anaemia -- a shortage of red blood cells. Anaemia causes people to become pale, weak, and fatigued.

Multiple myeloma can also cause the level of platelets in the blood to become low. This can lead to increased bleeding and bruising. The present research and its findings have been detailed in the July edition of the online journal PLoS One.