Research done at the Masonic Cancer Center at the University of Minnesota found the regulator of one of the three major cancer-causing genes, MYC. 

The discovery found that the gene is amplified to abnormal levels by a non-coding RNA, PVT1, creating cancerous cells. This revelation occured in August of 2012, but its recent publication into the internationally renowned Journal of Science, Nature, is likely to propel further research. 

 “It [The partnership of MYC and PVT1] forms this vicious cycle in which the MYC protein become boosted, become abnormal, and then cells become cancerous,” lead researcher Dr. Anindya Bagchi said.

What makes the research most difficult, Bagchi said, is that humans need the MYC gene for our cells to survive, but at normal amounts. There becomes a problem when abnormal amounts of MYC arise.

What the research showed was that if you can uncouple and break this cycle of MYC’s dependency on PVT1, then you can bring MYC to its precancerous level.

Graduate student and first author of the research Yuen-Yi Tseng described their research process as chromosome engineering, where they built their own genes using mice as their model before exploring human cancer cells.

Tseng said creating and growing the engineered cells was very detailed work. She worked with the mice for two years, Dr. Bagchi said.

As of now, the team is expanding their focus to all solid tumors, including cancers from the lungs, prostate, brain, head and neck. In total the team has tested the cells of 25 difference cancers, all of which have displayed the same phenomena.

Another area of research is diagnosis. They will be testing cells from one kind of cancer, but at different stages of its development, in order to potentially use PVT1 as a way to diagnose different stages of other cancers. Ideally doctors would be able to watch for the PVT1 and MYC partnership to identify what stage certain cancers are at.

 “Our hypothesis is that somehow, somewhere during the formation of cancer, MYC is an essential component, even in non-MYC–driven cancers,” Bagchi said. This is significant if they want to expand drug therapy or diagnoses potentials to cancers beyond just MYC-driven cancers.