first steps in formation of pancreatic cancer identified
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November 10, 2014
Mayo Clinic
The first steps in the origin of pancreatic cancer have been identified byresearchers who say that their findings suggest preventive strategies toexplore. The scientists described the molecular steps necessary foracinar cells in the pancreas -- the cells that release digestive enzymes -- to become precancerous lesions. Some of these lesions can thenmorph into cancer.
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Shown is a region of a pancreas with preneoplastic lesions. Red labeling indicatesmacrophages, green labeling indicates pancreatic acinar cells that dedifferentiate,and grey labeling indicates further progressed pancreatic lesions.
esearchers at Mayo Clinic's campus in Jacksonville say they haveidentified first steps in the origin of pancreatic cancer and that theirfindings suggest preventive strategies to explore.
In an online issue of Cancer Discovery, the scientistsdescribed the molecular steps necessary for acinarcells in the pancreas -- the cells that release digestiveenzymes -- to become precancerous lesions. Some ofthese lesions can then morph into cancer.
"Pancreatic cancer develops from these lesions, so ifwe understand how these lesions come about, we maybe able to stop the cancer train altogether," says thestudy's lead investigator, Peter Storz, Ph.D., a cancerbiologist.
The need for new treatment and prevention strategies ispressing, Dr. Storz says. Pancreatic cancer is one of the most aggressive humancancers -- symptoms do not occur until the cancer is well advanced. One-year survivalafter diagnosis is only 20 percent. It is the fourth leading cause of cancer death in this
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The scientists studied pancreatic cells with Kras genetic mutations. Kras produces aprotein that regulates cell division, and the gene is often mutated in many cancers.More than 95 percent of pancreatic cancer cases have a Kras mutation.
The researchers detailed the steps that led acinar cells with Kras mutations totransform into duct-like cells with stem cell-like properties. Stem cells, which candivide at will, are also often implicated in cancer.
They found that Kras proteins in the acinar cells induce the expression of a molecule,ICAM-1, which attracts macrophages, a specific kind of immune cells. Theseinflammatory macrophages release a variety of proteins, including some that loosenthe structure of the cells, allowing acinar cells to morph into different types of cells.These steps produced the precancerous pancreatic lesions.
"We show a direct link between Kras mutations and the inflammatory environment thatdrive the initiation of pancreatic cancer," Dr. Storz says.
But the process can be halted in laboratory mice, he adds. "We could do this twoways -- by depleting the macrophages or by treating the transformed cells with ablocking antibody that shuts down ICAM-1," says Dr. Storz. "Doing either one reducedthe number of precancerous lesions."
Dr. Storz noted that a neutralizing antibody that blocks ICAM-1has already beendeveloped. It is being tested for a wide variety of disorders, including stroke andrheumatoid arthritis.
"Understanding the crosstalk between acinar cells with Kras mutations and themicroenvironment of those cells is key to developing targeted strategies to prevent andtreat this cancer," he says.
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The above story is based on materials provided by Mayo Clinic. Note: Materials maybe edited for content and length.
Journal Reference:
1. G.-Y. Liou, H. Doppler, B. Necela, B. Edenfield, L. Zhang, D. W. Dawson, P. Storz.Mutant Kras-induced expression of ICAM-1 in pancreatic acinar cells causesattraction of macrophages to expedite the formation of precancerouslesions.. Cancer Discovery, 2014; DOI: 10.1158/2159-8290.CD-14-0474
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