Researchers from the Mayo Clinic confirmed in new research that more than one oncogene is needed to trigger pancreatic cancer, and the second factor creates a "perfect storm" that allows tumors to form. The paper, published in the September 10 issue of Cancer Cell, subverted the current view that KRAS oncogene mutations are sufficient to trigger pancreatic cancer and unlimited cell growth.
The findings reveal some key clues about the mechanism of pancreatic cancer formation and the reasons why only a few patients benefit from current treatment. The findings also provide some ideas on how to improve treatment and prevent pancreatic cancer.
The research team was led by Dr. Howard C. Crawford, a cancer biologist at the Mayo Clinic, and Dr. Jens Siveke, Munich University of Technology, Germany. The researchers found that for the formation of pancreatic cancer, the mutant KRAS must recruit a second participant: epidermal growth factor receptor EGFR. The third genetic participant, Trp53, makes pancreatic cancer very difficult to treat.
Scientists have also discovered that the EGFR required for pancreatic cancer is triggered by pancreatitis.
"We believe that the perfect storm that triggers pancreatic cancer includes KRAS mutations and organ inflammation, and then they work together to turn on EGFR," Crawford said.
He said: "The bottom line is that without EGFR, the tumor will not form-this was not known before this study. We also think that inflammation in the pancreas has a great effect on turning on EGFR."
The researchers found that when they blocked EGFR activity, the study mice prevented the formation of chronic pancreatitis and pancreatic cancer.
They further found that in mice that lost the expression of TP53 tumor suppressor (this is the case in up to 60% of human pancreatic cancer cases), the tumor avoided the dependence on EGFR to initiate pancreatic cancer formation and continued growth.
Pancreatic cancer is a highly fatal disease, and there are currently no drugs that can target the mutant KRAS protein. Dr. Crawford said the research suggests that some patients, such as those with chronic pancreatitis, may be good candidates for EGFR inhibitor therapy to fight or prevent pancreatic cancer.
"The clinical significance of this study is exciting. It shows that patients with pancreatic cancer with normal p53 activity and patients with chronic pancreatitis may be good candidates for EGFR inhibitor therapy," said Dr. Crawford.
The EGFR inhibitor erlotinib is part of the standard treatment for patients with pancreatic cancer, but overall it has a minimal effect in the patient population, he added: "This may be because many patients are likely to have TRP53 tumor suppression Mutation, so erlotinib cannot help them, because tumor growth no longer requires EGFR. "
He said: "Maybe erlotinib or other EGFR inhibitors can work better in patients without TRP53 mutations. We also believe that this drug can prevent the formation of pancreatic cancer in patients with chronic pancreatitis, chronic pancreatitis is An important risk factor for pancreatic tumor formation. "
Dr. Crawford said: "These findings give us some very important clues about the mechanism of pancreatic cancer formation and progression. The more we know about these early tumors, the more we can devote ourselves to diagnosis and treatment."
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