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Cancer-causing Protein May Heal Damaged Spinal Cord And Brain Cells

Date:
June 29, 2006
Source:
Columbia University Medical Center
Summary:
Cancer researchers at Columbia University Medical Center have found that a protein known for driving the growth of cancer also plays a surprising role in restoring the ability of neurons to regenerate, making it an important target for addressing spinal cord damage or neurological diseases like Alzheimer's.

Cancer researchers at Columbia University Medical Center have found that a protein known for driving the growth of cancer also plays a surprising role in restoring the ability of neurons to regenerate, making it an important target for addressing spinal cord damage or neurological diseases like Alzheimer's.

The research will be published in the journal Nature and will be available Wednesday, June 28 on the journal's web site.

"Our finding suggests that the same process this protein uses for proliferating cancer could also potentially be used to regrow axons that are damaged in spinal cord injuries or neurological diseases," said Antonio Iavarone, M.D., associate professor of neurology and pathology at Columbia University Medical Center's Institute for Cancer Genetics, and the study's lead author.

The proteins – known as Id proteins - are abundant in the cells of many different types of cancer, including brain, breast cancer and pediatric tumors, and were known to promote tumor growth and aid in the spread of cancer.

While searching for ways to attack Id's cancer-causing properties, Dr. Iavarone and Anna Lasorella, M.D. assistant professor of pediatrics and pathology at the Institute for Cancer Genetics, discovered the surprising neuron-healing properties of Id proteins.

Their initial findings, also published in the Nature paper, are significant for potential cancer therapies. The researchers found that an enzyme inside normal cells - called APC – usually degrades Id proteins soon after they're produced, but cancerous cells show a very high level of Id proteins. This suggests that re-introducing the APC enzyme into cancer cells could eliminate the proteins and arrest the growth of tumor cells – something that researchers will now investigate.

Spurring Neuronal Regrowth

Among neurons, however, Dr. Iavarone and Dr. Lasorella examined the Id protein potential for promoting growth, rather than arresting it. The researchers wanted to use the power of Id proteins to stimulate growth of axons - the structures on neurons responsible for transmitting electrical signals in the brain and spinal cord. But to do that they needed to overcome the problem of the APC enzyme, which degrades the protein in normal cells. So they constructed a "super" Id protein that would resist degradation from the APC enzyme, allowing it to promote axonal growth.

Normally neurons cannot regenerate damaged axons because of the presence of myelin, a substance that surrounds the axons, but the degradation-resistant "super" Id protein was able to promote axon growth even in the presence of myelin.

Dr. Iavarone added that there is no chance that such a therapy would cause cancer in the brain or spinal cord. "Neurons have completely lost the ability to create new cells so there's no danger of creating a tumor. The only growth they're capable of is regeneration of their axons," he said.


Story Source:

The above story is based on materials provided by Columbia University Medical Center. Note: Materials may be edited for content and length.


Cite This Page:

Columbia University Medical Center. "Cancer-causing Protein May Heal Damaged Spinal Cord And Brain Cells." ScienceDaily. ScienceDaily, 29 June 2006. <www.sciencedaily.com/releases/2006/06/060629085823.htm>.
Columbia University Medical Center. (2006, June 29). Cancer-causing Protein May Heal Damaged Spinal Cord And Brain Cells. ScienceDaily. Retrieved July 23, 2014 from www.sciencedaily.com/releases/2006/06/060629085823.htm
Columbia University Medical Center. "Cancer-causing Protein May Heal Damaged Spinal Cord And Brain Cells." ScienceDaily. www.sciencedaily.com/releases/2006/06/060629085823.htm (accessed July 23, 2014).

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