CANBERRA, Australia — Perhaps the most notorious of all diseases and ailments, cancer is an incredibly hard condition to treat. One of the main reasons cancer has proven so difficult to “crack” for modern medicine is the fact that it excels at evading the immune system. Another of cancer’s key features is the disruption of normal gene regulation, which causes cancer cells to both appear and behave differently than normal, healthy cells.
Now, potentially groundbreaking research by a team at the Australian National University (ANU) and the Peter MacCallum Cancer Centre has discovered that a specific protein, called Menin, can contribute to the abnormal deactivation of specific genes in cancer cells.
Researchers explain that cancer cells are capable of turning off certain genes, or ensuring they remain in a dormant state. When certain immune genes are deactivated, some cancers are then able to evade detection by the immune system — essentially becoming invisible. Such a development, of course, can allow a tumor to continue growing unimpeded.
Through the targeting of the Menin protein with drug therapies, study authors believe they can reactivate these genes. That means the cancer cells would once again become visible, opening the door for the immune system to seek out and destroy them.
All in all, this work could very well lead to new, more successful treatments for cancers like lymphoma and lung cancer. Moreover, Professor Mark Dawson, from the Peter MacCallum Cancer Centre, adds these findings can help scientists learn more about how cells function in general.
“Our research discovery has major implications for many different fields of research because we need to understand how cells make decisions and change the way they act in order to find new ways to treat cancer,” Prof. Dawson says in a university release.
Gene editing could wipe out cancer’s ability to stay invisible
ANU Associate Professor Marian Burr, one of nine Snow Fellow researchers and a joint senior author, adds scientists utilized gene-editing technology to delete the Menin protein from cancer cells.
“Menin has been previously shown to activate genes. However, our research unexpectedly found that Menin functions to keeps these genes in an inactive dormant state,” Burr explains. “This meant that by deleting Menin we could turn on the immune genes, which is essential to help the immune system to detect and kill the cancer cells.”
“Importantly, specific drugs that inhibit Menin have been developed and are currently being tested in clinical trials for specific forms of leukemia,” she concludes. “Our findings expand the potential clinical uses of these drugs. We have shown that Menin inhibitors can be used in combination with other existing treatments to enhance killing of lymphoma and lung cancer cells in the laboratory.”
Study authors note that they believe these drugs have great potential to prove effective against other types of cancer as well.
The study is published in Nature Cell Biology.
