Caspase-2 May Be Important In Suppressing Lymphoma

Researchers have found that a specific gene plays an important role in suppressing lymphoma, a type of blood cell cancer.

AsianScientist (Nov. 29, 2013) – Researchers have found that a specific gene plays an important role in suppressing lymphoma, a type of blood cell cancer.

Caspase-2 was first discovered almost 20 years ago by University of Adelaide Professor Sharad Kumar, co-Director of the Center for Cancer Biology within SA Pathology. The caspase-2 gene is related to a family of proteins that are essential for the self-destruction of cells in the body, a process known as apoptosis.

For the past two decades, Professor Kumar’s laboratory has been investigating the processes by which cells commit suicide and the molecular machinery that determine whether a cell lives or dies. Cell death is essential to maintain the correct number of cells in the body and to delete cells that have been damaged and become potentially harmful.

“Cell death and survival are controlled by a large number of genes, and aberrations in these genes are often linked to diseases. For example, an ability for cells to evade apoptosis is a well-known hallmark of cancer,” said Professor Kumar.

In new findings published in the Proceedings of the National Academy of Sciences, Professor Kumar and his team found in laboratory studies that expression of caspase-2 could prevent tumor formation.

“It does this by ensuring that cells predisposed to cancer maintain a healthy number of chromosomes,” said Professor Kumar. “By some unknown mechanism, caspase-2 appears to prevent cells from losing and gaining copies of the chromosomes, which is a trait frequently observed in tumor cells.”

“This research not only provides new information on the development of cancer, it also defines how caspase-2 can potentially work as a tumor suppressor gene. This is an exciting finding and one that we’re already investigating further,” he said.

The article can be found at: Puccini J et al. (2013) Loss of caspase-2 augments lymphomagenesis and enhances genomic instability in Atm-deficient mice.

Source: The University of Adelaide; Photo: euthman/Flickr/CC.
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