Pancreatic cancer 'time machine' reveals tumor development and invasion

Pancreatic cancer has one of the worst survival rates among cancers. Patients can expect as low as a 9% chance to live for at least five years after being diagnosed.

Going back in time to observe how cells with key gene mutations interact and become invasive would help researchers better understand how the cancer starts and identify it sooner.

A pancreatic cancer "time machine" engineered by Purdue University researchers has revealed that the disease is even more unpredictable than previously thought: Cancer cells promote each other's invasiveness when they grow together.

The study, published in the journal Small, is just the beginning of a new discovery about how pancreatic cancer evolves. Since the paper's publication, the researchers also have found drug resistance in cancer cell types originating from two drug-sensitive ones.

The time machine is a hollow tube of collagen that realistically mimics the microanatomy of a pancreatic duct. By injecting cancer cell lines into microfluidic channels within the artificial duct, the researchers can use the system as a model for observing how pancreatic cancer behaves over time.

Typically, it takes 10-20 years for pancreatic cancer to develop in a patient. Even in an animal model, the process is several months long. This pancreatic tumor model condenses cancer development to just two weeks.

We can observe what happens over a long period of time. This helps us to see trends that we wouldn't normally see." Bumsoo Han, Purdue professor of mechanical engineering

Bumsoo Han builds models for studying how cancer cells move in biological systems.

The tumor model speeds up time because researchers can load in cell lines from an animal model or patient without waiting for gene mutation to happen first. The life-like structure of the tumor model allows the researchers to reconstruct the mutation as it would happen in the body.

To go back in time, the researchers just rewind footage taken by imaging equipment from the side of the artificial duct.

For this study, a group led by Stephen Konieczny, a professor of biological sciences at Purdue, developed the pancreatic cell line in a mouse model. Han's team then loaded the cell line through the microfluidic channels of the artificial pancreatic duct. Once inside, the cell lines fill the duct and start growing.

What makes the tumor model so realistic is its shape.

"The curvature of the pancreatic duct affects the behavior of cells. We could culture these cancer cells on a petri dish, but because the dish is flat, we wouldn't see the same behavior," said Han, who is the program leader of the Purdue University Center for Cancer Research and has a courtesy appointment in biomedical engineering.

The researchers saw that after two different cancer cell types merged into the pancreatic tumor model device, these cells became more invasive and sprouted from the duct to form tumors.

Since cancer is technically a group of diseases, and pancreatic cancer involves four major driver mutations, Han's team plans to further explore how each of these mutations interacts with each other. The tumor model also can be used as a prescreening tool to discover new drug targets for better drugs, Han said.

A patent has been issued for the pancreatic tumor model via the Purdue Research Foundation Office of Technology Commercialization.

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Hypersensitivity to pain produced by early life stress gets worse by later stress exposure

Early-life stress such as childhood neglect and abuse is suspected to contribute to the development of chronic pain in adulthood, a new study has suggested.

Researchers  used an animal model of maternal neglect that stresses rat mothers by restricting nesting/bedding material.

These stressed rat mothers do not provide consistent levels of nurturing to their pups, i.e., the mothers are present but their care is unpredictable, resulting in increased levels of stress in the pups. The pups were otherwise not harmed or stressed.

Pups that had experienced this early-life stress showed increased reactivity to painful stimuli, particularly if they were exposed to a mild stress, an unpredictable unpleasant noise, as adults.

This enhanced muscle pain was related to both catecholamines, natural compounds in the body involved in the “fight-or-flight” response, and cytokines, molecules involved in the body’s inflammatory response system.

Interestingly, interventions that blocked the actions of the catecholamines and cytokines reduced the sensitivity to pain in the stressed pups.

Dr. said that while it has been recognized for some time that early life events can shift homeostatic balance, predisposing adults to the development of chronic pain, that this could be mediated by a peripheral mechanism, involving the interaction between immune and neuroendocrine stress axes suggests novel approaches to detecting individuals at risk as well as to treatment of chronic pain.

This study suggests a ‘two hit model’ for the risk for pain syndromes: an initial stressor that predisposes to increased reactivity to later stress. The authors implicate both stress response and inflammation systems in the body in the link between stress and pain, potentially pointing to new treatment mechanisms.

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