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Scientists identify link between stem cell regulation and the development of lung cancer
Date:6/19/2014

themselves, which causes the cells not to mature and instead become precancerous lesions. Subsequent progressive genetic changes to the cells in these lesions over time can eventually allow cancerous tumors to form.

"Low ROS is what keeps stem cells primed so that your body is poised and ready to respond to injury and repair," said Gomperts, who also is an associate professor in the department of pediatrics at UCLA. "Loss of this ROS regulation leads to precancerous lesions. Now, with this precancerous model in place, we can begin looking for what we call 'driver mutations,' or those specific changes that take the precancerous lesions to full-blown cancer."

Gomperts said that because many different factors including cigarette smoke, smog and inflammation could potentially trigger an increase in ROS in the airway stem cells, researchers might eventually be able to customize treatments based on the cause. "There are likely multiple ways for a person to get to a precancerous lesion, so the process could be different among different groups of people. Imagine a personalized way to identify what pathways have gone wrong in a patient, so that we could target a therapy to that individual."

The research's ultimate goal is to develop a targeted strategy to prevent pre-malignant lesions from forming by targeting the biology of these lesions and therefore preventing lung cancer from developing.

"Our study is important because it sheds light on how lung cancer can form, and this will hopefully lead to new therapies for this terrible disease," Paul said.

The UCLA study also is noteworthy for finally identifying specifically how ROS affects the proliferation of stem cells.


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Contact: Shaun Mason
smason@mednet.ucla.edu
310-206-2805
University of California - Los Angeles
Source:Eurekalert

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