Scientists have in fact identified a new key player in the development of this cancer: the MICAL2 enzyme. This protein, usually involved in the movement and morphology of cells, turns out to be a real fuel for pancreatic tumors.
The authors actually observed 3 elements:
Among patients undergoing surgery to remove pancreatic ductal adenocarcinoma, those whose tumor cells had low expression of MICAL2 survived twice as long as those whose tumor cells produced more. This suggests that MICAL2 could be involved in the progression of the disease to an advanced stage; The KRAS protein is known to be often involved in the emergence of cancer. It stimulates the growth of cancer cells. But deactivating the MICAL2 gene would significantly slow down KRAS activity. When tumor cells are deficient in MICAL2, the KRAS signaling pathway is unable to harvest nutrients that lead to tumor growth; MICAL2 is thought to facilitate the spread of cancer to other healthy organs.
The authors have no doubt that this enzyme could be a promising target for drug therapies against pancreatic ductal adenocarcinomas. “Pancreatic cancer has the highest mortality rate of all common cancers and current treatments are woefully inadequate,” says Professor Andrew Lowy, division chief of surgical oncology at the University of San Diego. “We believe it will be possible to target MICAL2 with drugs because it is an enzyme belonging to a class of proteins against which inhibitor drugs have already been successfully developed to treat other human diseases. We are currently working to identify drug candidates to begin blocking MICAL2 function in pancreatic cancer. »
Why does my throat hurt in the morning?
Source: Destination Santé
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