Researchers Found A Way To Stop Tumors From Developing

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Researchers believe that they found the “Achilles Heel” of cancerous tumors based on tests performed in both human and rodent cells, and we already have the drug to target the said weakness in tumors.

Today, a study published in Nature Cell Biology from the Perelman School of Medicine of the University of Pennsylvania, discovered the identity of a new path in a tumor’s growth; whereas altering it could overall prevent tumors from developing.

The new pathway is that of a protein called Activation Transcription Factor 4 or ATF4. Researchers said that the chemical pathway works in tandem with the gene called MYC — a gene that researchers have been trying to target to prevent cancerous tumors from developing.

Normal MYC genes control healthy cell growth. However, some of these genes can mutate or become too abundant that results in a chain reaction that helps tumors undergo uncontrollable growth and spread.

There is currently no specific way to target MYC directly; however, so as a workaround, researchers focused other pathways indirectly hoping it could impede tumor growth.

Constantinos Koumenis, Ph.D., the Richard Chamberlain Professor of Radiation Oncology, vice chair and research division director of Radiation Oncology, and the lead researcher on the latest study, believed that they needed a more direct approach toward MYC to effectively attack the tumor-causing genes.

“What we’ve learned is we need to go further downstream to block tumor growth in a way that cancer cells can’t easily escape, and our study identifies the target to do just that.”

In the experiment conducted by the researchers, they discovered that the MYC gene converged with the ATF4 in its chemical pathway. In theory, they believed that by targeting the ATF4 protein, they would also be directly attacking the illusive MYC gene.

Putting the theory in practice, researchers used lab-grown human lymphoma-causing cells as well as human breast and bowel cells. Meanwhile, they used rodents that are genetically engineered to develop lymphomas to test the theory on live subjects.

In both groups — cells developed in the lab and rodents — researchers knocked out the ATF4 protein. Meanwhile, MYC continued to work with ATF4 but eventually died.

Notably, the ATF4 protein activates MYC’s needs to support and develop cells, and it also controls the rate at which cells make specific proteins called 4E-BP.  However, with the protein rendered “unconscious,” MYC continued to produce an abundance of 4E-BP proteins that led to its eventual death due to stress.

As a result, the findings of the study showed that lymphomas and bowel tumors growing in mice stopped while the human tumor cells driven by MYC had an abundantly increasing amount of both ATF4 and 4E-BP.

“This shows us the potential impacts of targeting ATF4 in MYC-dependent tumors, something we’re already studying. We’re also working to confirm this approach will not cause any serious off-target effects,” said lead author Feven Tameire, Ph.D., who conducted this research while she was a doctoral candidate at Penn.

As of the moment, we have available inhibitors in the market that can cease the production of ATF4 — linked to a host of diseases, including Parkinson’s and Alzheimer’s.

However, researchers cannot wholly implement these inhibitors to treat people developing tumors, as further research needs to be conducted.

The discovery does, however, shed light into the understanding of how tumors grow and develop in the human body. Future studies are expected to look farther into ATF4’s connection with tumors and how they can be manipulated to prevent cancer from developing overall.

The study comes after a team from Cold Spring Harbor Laboratory proposed a different way to target MYC-driven cancers. This team, on the other hand, is looking to target a different protein called PHLPP22 to target MYC.

Meanwhile, other biotech startups are still approaching MYC indirectly. Aptos Biosciences, for example, is conducting early-stage human trials of its MYC inhibitor, APTO-253.

So far, Koumenis’ team showed the best potential in targeting the MYC gene and ultimately preventing tumors.

The International Agency for Research on Cancer estimates about 18 million people a year are diagnosed with the disease — which claims around 10 million lives annually.

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