A newly discovered molecule could lead to a cure for pancreatic cancer
It's the dreaded C-word: Cancer. Some dare not even say it in case it happens to them.
Now, a research team led by scientists at Roswell Park Comprehensive Cancer Center may have made a significant breakthrough in treating pancreatic cancer, according to a press release published by the institute on Wednesday.
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The mighty MMRi62 molecule
It all comes down to one molecule: MMRi62. This specific and newly-discovered molecule targets and kills cancer cells and the harmful proteins that encourage their growth and spread, an impressive feat that could lead to a promising cure.
Pancreatic cancer cells, also known as pancreatic ductal adenocarcinoma (PDAC) cells, are already prone to experiencing ferroptosis, a death triggered by iron. Therefore researchers have dedicated their time to the identification of novel agents that induce ferroptosis.
“MMRi62 causes degradation of an iron-storage protein called FTH1, as well as a protein that is mutated in PDAC, resulting inhibition of metastasis and ferroptosis, a form of cell death triggered by free cellular iron,” said in the statement Xinjiang Wang, Ph.D., Associate Professor in the Department of Pharmacology and Therapeutics at Roswell Park.
A cancer cell death triggered by iron
PDAC is so devastating because of certain mutations in the KRAS and TP53 genes which make tumors very resistant to chemotherapy. Currently, there are no treatments available for these mutations and the disease has a poor 5-year survival rate of only 12 percent. This could, however, soon change!
“We showed through this study that in a preclinical model, MMRi62 is capable of inducing ferroptosis in PDAC cells harboring either KRAS or TP53 mutations, which in turn inhibited tumor growth and prevented metastasis of tumors to distant organs,” added Dr. Wang. “Although no ferroptosis-inducing agents are currently available, our hope is that our discovery will lead to promising new MMRi62-based treatments for recalcitrant cancers such as PDAC.”
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