Photo taken on July 3, 2016 shows a child receiving medical treatment at a children's cancer hospital in Cairo, Egypt. (Xinhua/Ahmed Gomaa)
WASHINGTON, July 2 (Xinhua) -- Scientists have discovered a new weakness of cancer, which forces tumor cells to over-stress and self-destruct.
Cancer tumors are groups of abnormal cells that form lumps or growths. They can start in any part of the body. Survival depends on the growth and size of the tumor and the area affected.
For years, scientists have been trying to target a gene called MYC that is known to drive tumor growth in multiple cancer types when it is mutated or over-expressed.
A team of scientists at the University of Pennsylvania announced that they have identified a new pathway that works as a partner to MYC and may be its Achilles' Heel, according to their findings recently published in the journal Nature Cell Biology.
The pathway involves a protein called ATF4, and by blocking this protein that fuels tumors kills them off.
Photo taken on Feb. 4, 2016 shows an X-ray film of a patient suffering from sinonasal cancer at a hospital in Jakarta, capital of Indonesia. (Xinhua/Veri Sanovri)
"What we've learned is we need to go further downstream to block tumour growth in a way that cancer cells can't easily escape, and our study identifies the target to do just that," said co-senior author Professor Constantinos Koumenis.
Researchers found that when they knocked out ATF4 in cells or mice, tumor cells continued to build up those proteins and eventually died as a result of stress. This blocked tumor growth in mice with lymphomas and colorectal cancer, which is evidence that these findings may point to an approach that could work for humans.
"We're also working to confirm this approach will not cause any serious off-target effects," said lead author Doctor Feven Tameire.
Future studies will also focus on continuing to investigate why ATF4 works the way it does, which may help their understanding of whether there are other potential targets in the chain, researchers said.