Pancreatic cancer is a tough nut to crack. It’s one of those diseases that doctors often find too late. It’s also a leading cause of death from cancer.
In fact, only 12 out of 100 people diagnosed with this type of cancer live beyond five years. It’s a grim statistic, but a team of international researchers has recently made some ground-breaking discoveries.
They’ve given us new insight into how this cancer begins and grows. The team from the Sloan Kettering Institute at Memorial Sloan Kettering Cancer Center (MSK) and IRB Barcelona published their findings in Science.
The Story of Mutations
Cancer is often linked to gene mutations. These are changes in our DNA that alter how our cells behave. One such mutation occurs in a gene called KRAS.
This gene normally controls cell growth. But when it’s mutated, it goes into overdrive. This mutation is common in pancreatic cancer, as well as lung and colorectal cancers.
The Bigger Picture: Mutations Plus External Factors
However, it’s not just about mutations. There’s more to the story. Other factors, like injury causing inflammation, also play a big part.
This inflammation can change the cells and their surroundings in ways that help cancer grow.
For instance, in pancreatic cancer, these changes happen quickly, sometimes within a day or two of tissue damage.
The changes also make cells much better at communicating with each other. This communication is a big part of how cancer progresses.
The Study: Making Sense of the Early Stages of Cancer
The researchers wanted to understand the early stages of pancreatic cancer.
They used advanced technology and computer methods to study the very first changes in cells that lead to pancreatic ductal adenocarcinoma (PDAC). PDAC is the most common type of pancreatic cancer.
To do this, they used genetically engineered mice that could mimic human pancreatic cancer. This allowed them to see how normal cells change and become cancerous.
Cells Changing Their Identity: Cell Plasticity
One of the key findings was about something called cell plasticity. This is the ability of a cell to change its identity. Think of it as a kind of shapeshifting.
The researchers found that inflammation increases this shapeshifting ability in precancerous cells.
These shapeshifting cells can send and receive more signals than a normal cell. They found that these changes weren’t random.
They happened in the same way in different mice. This suggests that this process is predictable, and therefore, possibly controllable.
The Inner Workings of Cells
The researchers used a technique called single-cell analysis. This allowed them to study individual cells at different stages of cancer development.
They found that certain groups of cells became major communication hubs. These cells drove the progression of pancreatic cancer.
Using advanced computation, they developed a new way to measure the shapeshifting ability of a cell.
They also found that the shapeshifting cells had more genes related to communication. This increased communication ability changed the way these cells interacted with the immune system.
Linking Lab Findings to Real-World Applications
Understanding these early changes in cells could help doctors detect or even prevent pancreatic cancer before it becomes too advanced.
It also opens up the possibility of developing new treatments to slow down cancer progression.
In short, this study has given us a clearer picture of how pancreatic cancer develops. It’s a big step forward in our fight against this deadly disease.
But, as always, there’s more research to be done. We’re still learning about this complex disease, and every new discovery brings us closer to finding more effective treatments and, hopefully, a cure.
The study was published in Science.
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