Washington, Aug 28: Researchers have found that a gene which is crucial to the development and functioning of an entire family of immune cells, also holds the key to understanding why one member of that family can become cancerous.
Researchers at the St. Jude Children's Research Hospital and the Blood Research Institute at the Blood Center of Southeastern Wisconsin, Milwaukee, report the finding in the September issue of Nature Immunology.

The researchers had previously shown that one of these cell types, marginal-zone B cells, can give rise to a cancer called mucosa-associated lymphoid tissue (MALT) lymphoma when the cells abnormally over-express a gene called Bcl10. The current finding suggests that a drug that blocks the action of Bcl10 could be an effective treatment for this cancer.
They discovered that Bcl10 activates a pathway of molecular signals that drives antibody-producing B cells to mature into one of three different members of this family of immune system cells: follicular, marginal zone and B1 B cells.
Mice lacking Bcl10 have a significant decrease in mature B cells and cannot launch an effective antibody response against bacteria in their bloodstream. To learn how Bcl10 controls B cell development and function, the investigators studied mice in which the gene was inactivated.

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The mice produced nearly normal numbers of immature B cells. However, these cells did not mature normally. This showed that Bcl10 function is essential for B-cell development.
The researchers found that mice lacking a functional Bcl10 gene could not activate specific pathways of signaling molecules that belong to a family of proteins called NF-jB. The NF-jB proteins are normally activated by Bcl10 after B cells encounter invading organisms, such as bacteria. These proteins then cause B cells to fully mature and release antibodies targeted against those specific organisms.

The central role of Bcl10 in B cell development and function is further evidence that this gene is a major contributor to the development of MALT lymphoma.
Bureau Report