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Loss of cell's 'antenna' linked to cancer's development

, the discovery that too much HEF1 and Aurora A cause cilia to disassemble provides important hints into what may be happening in cancers.

Defects in cilia have already been identified in one disease that represents a significant public health burden. Polycystic kidney disease, or PKD, arises from genetic mutations that cause flawed kidney-cell ciliary signaling. PKD is the most common serious hereditary disease, affecting more than 600,000 Americans and 12.5 million people worldwide.

In this incurable syndrome, patients develop numerous, fluid-filled cysts on the kidneys. For many patients, chronic pain is a common problem. PKD leads to kidney failure in about half of cases, requiring kidney dialysis or a kidney transplant.

The proteins involved in dismantling the cilia are no strangers to Golemis and her team. Golemis has been studying HEF1 for over a decade, since she first identified the gene. She first discovered that HEF1 has a role in controlling normal cell movement and tumor cell invasion. Golemis laboratory has also shown that Aurora A and HEF1 interact to initiate mitosis (chromosome separation) during cell division.

Suggestively, many cancers produce too much of the Aurora A protein, including breast and colorectal cancers and leukemia. In 2006, excessive production of HEF1 (also known as NEDD9) was found to drive metastasis in over a third of human melanomas, while HEF1 signaling also contributes to the aggressiveness of some brain cancers (glioblastomas).

Now theres a new activity for these proteins at cilia, said co-author Elizabeth P. Henske, M.D., a medical oncologist and genetics researcher who studies the genetic basis of kidney tumors. This complex HEF1 and Aurora A function may mean the increased levels of these proteins in cancer affect cellular response to multiple signaling pathways, rather like a chain reaction highway accident.

Clinical Application

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Contact: Karen Mallet
Karen.Mallet@fccc.edu
215-728-2700
Fox Chase Cancer Center
28-Jun-2007


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