Susanna Fletcher Greer, Chief Scientific Officer of the V Foundation, shared a post on LinkedIn:
“What if some of the earliest steps toward cancer have less to do with a tumor forming and more to do with how our cells handle the normal wear and tear of being alive? A new study, “NADPH-producing enzymes restrict the formation of pancreatic precancerous lesions,” led by V Foundation grantee Dr. Costas Lyssiotis, and lab at the University of Michigan Medical School, takes us back to one of the very first moments in pancreatic cancer and shows that long before anything is visible, cells are already struggling to keep themselves balanced and protected from becoming cancerous. This is exactly the kind of high risk, high reward work supported the V Foundationsupports.
This kind of “stress” has nothing to do with how someone feels or what they are going through. It is built into how our cells work. Every cell is constantly making energy, repairing damage, and cleaning up the byproducts of those processes. Most of the time, this happens seamlessly. But when those internal cleanup systems start to fall behind, even slightly, it can create an environment where damage builds up and cells begin to drift off course.
In the pancreas, cells have a natural ability to switch into a temporary repair mode after injury. It’s like a crew coming in to clean up after a storm. Normally, once the work is done, everything returns to normal, and the cleanup crew moves on. The same type of thing should happen in our pancreas cells. But in this study, Dr. Lyssiotis and team show that when cells cannot properly manage their internal damage, they can get stuck in that repair mode and begin forming early precancerous changes.
The process is like a city’s waste management system: if trash is collected regularly, a city runs more smoothly. But if the collection slows down, even a little, trash starts to pile up and the environment becomes, well, yucky. In cells in the pancreas, that buildup of damage can push them toward becoming cancerous.
This study opens the door to a set of questions that are directly relevant to patients. Like, if these early changes in how cells manage damage happen before a tumor forms, can we detect them? Researchers now will look for measurable signals of this imbalance, in blood and tissues, that could serve as early warning signs for pancreatic cancer when it is still at its most treatable stage.
It also raises the possibility of prevention. If we understand the systems that help cells stay balanced, we may be able to design strategies that support those systems before cancer develops. That could mean drugs designed to stabilize these processes, or identifying patients at higher risk and intervening earlier. At the same time, this work is a reminder that these systems are complex. More is not always better, and the right intervention must be matched to the right moment.
Another critical next step is understanding who this finding applies to. Pancreatic cancer is not one disease, and patients differ in their biology. We will need to study how these early changes vary across people and how they interact with other risk factors. That culmination of knowledge is what ultimately allows discoveries like this to move from the lab into real impact for patients.
For me, this is where the promise of this research really sits. It is not just about understanding how cancer grows, but about understanding how it begins. And when you can see the beginning more clearly, you create the opportunity to change the outcome entirely.
Find the Lyssiotis lab at Lyssiotis Lab | University of Michigan Medical School and read the paper at NADPH-producing enzymes restrict the formation of pancreatic precancerous lesions | Nature Metabolism.”
Other articles featuring Susanna Fletcher Greer on OncoDaily.