Researchers at the University of Texas Southwestern Medical Center have discovered that a protein once thought to be expressed in the brain only may play an important role in a deadly form of thyroid cancer as well as other cancers. This result may provide researchers with a new target to stop the progression of these cancers. Researchers found that over-activation of a certain protein in hormone-secreting cells helps fuel medullary thyroid cancer cells in mice as well as human cells. The over-active protein makes a potential target for inhibiting cancer cell growth.
These findings provide hope for other neuroendocrine cancers that occur outside the brain, for example, lung and pancreas. Albeit that medullary thyroid cancer is rare, it is often fatal.
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According to Dr. Fiemu Nwariaku, Professor of Surgery and a co-author on the paper, “Once or twice a month, patients come to UT Southwestern, often complaining of soreness or a swollen throat. When the diagnosis is a rare and incurable form of thyroid cancer called medullary thyroid carcinoma, it is always distressing for the patient – and for me – because we currently have no real therapies that truly extend life in these unfortunate cases”. At this time, treatment involves complete surgical removal of the thyroid and often surrounding tissues. Medullary thyroid cancer is often diagnosed late when it has already spread to other parts of the body.
Nwariaku points out that over two decades ago mutations in a gene were identified but this form represents about 25 percent of these cancers. Because of this information, genetic sequencing and screening are used as tools to diagnose and provide prognoses for families that carry the mutation. Nevertheless, causes for the other 75 percent of patients remains a mystery.
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Another lab in UT Southwestern’s Department of Psychiatry run by Dr. James Bibb, Associate Professor of Psychiatry and Neurology and Neurotherapeutics, were studying molecular mechanisms of brain disorders. Bibb and colleagues studying Alzheimer’s and other forms of dementia have developed a transgenic mouse model of brain injury by over-expressing the Cdk5 protein which was believed to be expressed only in brain. As the researchers observed the developing neurological symptoms, they noted that the mice became sick for some unknown reason. When they realized that all of the mice had developed that same thyroid cancer that Nwariaku treats, the mystery was resolved.
At that time, Bibb and Nwariaku partnered and began a study of both human and mouse thyroid cancer cells. What they found was that Cdk5 was present in thyroid C cells. They also report that the Cdk5 protein was able to escape cellular controls and cause cancer in both mice and humans. Now, along with other UT Southwestern investigators, Bibb and Nwariaku are progressing forward in their studies to develop new therapies to treat thyroid and other endocrine cancers. Together, the researchers are making use of high-throughput screening to identify molecules that block the Cdk5 pathway. At this time, there are two FDA-approved drugs for treating neuroendocrine cancers, however neither compound blocks the Cdk5 pathway.
Bibb notes that they are continuing research and identifying how Cdk5 causes growth and spread of certain cancers with the idea to develop new drugs which can be tested on their animal model. Down the road, they hope to go from lab bench to clinical trials.