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A new study by the Salk Institute, published July 24, 2019 in the journal Progress of science, shows that researchers could target these hard-to-treat cancers by looking for drugs that prevent a cell "switch", called CREB, from triggering tumor growth. The study was led by Marc Montminy, Professor and J.W. President of the Kieckhefer Foundation in Salk, in close collaboration with Professor Reuben Shaw, Director of the Salk Cancer Center and the William R. Brody Chair.
A drug that blocks this switch could have therapeutic benefits for patients with non-small cell lung cancer. This disease has escaped efforts to identify effective treatments. "
Marc Montminy, Professor and J.W. Chair of the Kieckhefer Foundation at the Salk Institute
Shaw adds, "There is not really any good treatment, so any idea that helps this subgroup of patients is a major breakthrough."
Scientists have studied CREB for decades. The molecule, known as the transcription factor because it binds to DNA to alter gene transcription, plays a key role in determining the proteins that a cell can make.
Montminy and Shaw Laboratories in Salk focused on the role of CREB in diabetic patients. Over the years, more and more research has suggested that CREB was important in cancer, but no one knew exactly how its influence on cancer growth – until recently.
Laura Rodón, a postdoctoral researcher at the Montminy Laboratory, wanted to examine the genes that CREB binds to patients with non-small cell lung cancer in order to understand its influence on cancer and to reveal potential new drug targets. . To do this, the team examined the growth of non-small cell lung cancer cell lines in a mouse model, studied tumors, and correlated the findings with tumor data in patients. They discovered that CREB and its partner, CRTC2, are activated in a subset of NSCLC tumors.
Normally, a tumor suppressor gene called LKB1 would block this activation – but this control point has disappeared in patients with the modified gene. In these patients, CRTC2 is abnormally activated and stimulates the genes that contribute to lung cancer. In particular, follow-up experiments have shown that CRTC2 mistakenly activates another gene called ID1, known to cause cancer in other tissues.
"It was an exciting discovery to show how CREB was ultimately contributing to this type of deadly cancer," Rodón said. "This suggests that if we could disable this CREB switch, we would be able to help patients."
The next step in this research is to look for drugs that may interfere with CREB or CRTC2 in this subset of patients with non-small cell lung cancer. Fortunately, previous studies to block CREB to help diabetic patients offer a range of new cancer treatment options. Shaw says that biomedical companies may have some promising non-small cell lung cancer drugs at hand and do not even realize it.
"There are a lot of interesting discoveries in this space," Shaw said. "Hopefully in the next two years we will know a lot more about the treatment of these patients."
The team agrees that this study is an excellent example of how Salk's labs work together to adopt new projects.
"Salk encourages collaborations," says Montminy. "It is therefore very easy to conduct such studies that require the collaboration of people with different skills."
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