Researchers identify first molecular steps that lead to pancreatic cancer

Date: Nov-10-2014 By identifying the molecular starting point when certain cells

in the pancreas become pre-cancerous lesions, researchers behind a new

study believe they have opened the door to exploring ways to prevent

the deadly disease.

Study leader Dr. Peter Storz, a cancer biologist at the Mayo Clinic

in Jacksonville, FL, who - with colleagues - describes the findings in the

journal Cancer Discovery, says:

"Pancreatic cancer develops from these lesions, so if we understand

how these lesions come about, we may be able to stop the cancer train

altogether."

Pressing need for new treatments and ways to prevent pancreatic

cancer

Cancer of the pancreas is one of the most aggressive human cancers and is the fourth leading cause of cancer death in the US.

Dr. Storz says there is a pressing need for new treatments and ways

to prevent pancreatic cancer, one of the most aggressive human cancers.

The disease is the fourth leading cause of cancer death in the US.

On average, patients with pancreatic cancer face a 20% chance of

living more than 1 year after diagnosis. The main reason for such a

poor prospect is that symptoms do not show until the cancer is well

advanced.

According to the National Cancer Institute, in 2014, over

46,400 people will be diagnosed with pancreatic cancer and over

39,500 will die of the disease.

For the study, the team investigated cells containing mutations of a gene that regulates a cell division protein. Called Kras, the gene is known to be mutated in over 95% of pancreatic cancer cases.

Study details steps that mutated cells follow as they transform

into pre-cancerous lesions

The researchers describe how they identified the detailed steps that

Kras-mutated acinar cells follow as they change into duct-like cells

with properties similar to stem cells - a type of cell often found in

cancer.

They noticed that Kras proteins in the acinar cells switched on a

molecule called ICAM-1. This in turn attracts macrophages -

inflammatory immune cells that release a variety of proteins, including

some that loosen the pancreatic cell structures. When they become

looser, the acinar cells then transform into different types of cell -

including the type that leads to pre-cancerous lesions.

Dr. Storz says their study shows a "direct link between Kras

mutations and the inflammatory environment that drive the initiation of

pancreatic cancer."

Team found two ways to stop process toward pre-cancerous lesions in

mice

The team also found they could halt the process in mice. They did

this in two ways. One way was by depleting the macrophages, and the

other way was by blocking the transforming cells with an antibody that shuts

down ICAM-1.

"Doing either one reduced the number of precancerous lesions," says

Dr. Storz, noting that an antibody that blocks ICAM-1 has already been

developed and is currently being tested for treating stroke, rheumatoid

arthritis, and other ailments.

He also says the key to developing targeted ways to prevent and

treat pancreatic cancer will be understanding "the crosstalk between

acinar cells with Kras mutations and the microenvironment of those

cells."

The National Institutes of Health funded the research.

The study follows another recent report from Medical News

Today about the prospect of a

simple blood test for pancreatic cancer, as more potential

biomarkers for the disease emerge.

Written by Catharine Paddock PhD

Not to be reproduced without permission.

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Courtesy: Medical News Today Note: Any medical information available in this news section is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional.