New Avenue to Eradicating the #1 killer Cancer

Researchers from the University of Florida have found that a protein known as Bc12 (found in high levels in lung cancer patients who smoke) actually helps cancer cells in the lungs to resist chemotherapy and to live much longer than they normally would, following subjection to chemotherapy. The study, published in the February 29 edition of the journal Molecular Cell explains how the protein does this by blocking the ability of healthy cells to repair themselves following damage by radiation or chemicals (such as nicotine).

"This will probably help us in the future find ways to prevent tumors," said Dr. Xingming Deng, assistant professor in the university's College of Medicine, adding that the protein could be a target for drug development. "We can target this mechanism and somehow find a way to prevent tumor formation."

This research is so crucial due to the unfortunate prevalence of lung cancer amongst cancer types. Lung cancer accounts for more deaths than breast, colon, and prostate cancers combined, and will account for about 29% of cancer deaths in 2008, according to the American Cancer Society. This amounts to nearly 162,000 people dying from lung cancer this year.

"Lung cancer is the No. 1 killer of all cancer types; it is the most dangerous," Deng said. "We wanted to find a way to treat lung cancer, how to prevent lung cancer, because lung cancer prognosis is very poor."

In the past, research conducted at the University of Florida identified nicotine as an activator of the protein. The new study provides information on how the protein is able to avoid the body's efforts to repair or kill cancer cells. The scientists were able to illuminate the molecular process by which Bc12 is able to disrupt the repair of damaged DNA in lung cancer cells, and were thus able to come up with their newest conclusion concerning Bc12's role in propagating the survival of cancerous lung cells.

"If a cell experiences DNA damage, often that DNA can be repaired. But we found that Bc12 can block the DNA repair mechanism, which promotes tumor formation and genetic instability. This is a very important fundamental mechanism that explains why this protein has (a cancer-forming) function," said Deng.

Cancer is marked by the buildup of genetic abnormalities in cellular chromosomes. Cells have natural processes by which they attempt to repair, or, (if unsuccessful) kill damaged cells. If these natural processes are impeded, as they were found to be by Bc12, these mutated cells will continue to live and multiply, propagating these dangerous mutations to create dangerous tumors. According to the researchers, it takes just one cell with this affliction to lead to tumor progression.

Future research prospects by Deng include investigation of the possibility of increasing the effectiveness of chemotherapy by blocking nicotine-induced Bc12 activation.

Written by Falishia Sloan

Reviewed by Brittany Raffa

Published by Pooja Ghatalia

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