Pancreatic cancer:

Share on Pinterest Researchers are continuing to research new treatments for pancreatic cancer, especially those that could slow down the spread of the disease. In a recent study, researchers discovered a way that pancreatic cancer cells communicate with each other. This communication allows the cancerous cells to grow faster and spread throughout the body. When the scientists blocked this communication pathway, the cancer slowed down. They believe that blocking this pathway could lead to better treatments for patients with pancreatic cancer.

The team of researchers used human tissue samples and genetically modified mice to discover how pancreatic cancer cells communicate. Their findings showed that pancreatic cancer cells release proteins called TGFβ1 and SDF-1. These proteins activate receptors on nearby cells and cause them to send signals to neighboring cells. The researchers tested whether blocking the signaling pathways affected the growth of pancreatic tumors in mice. They injected mice with pancreatic cancer cells that had been engineered to produce high levels of TGFβ1 and/or SDF-1. Mice that received injections of cells that produced both factors grew tumors much slower than mice that received injections of either factor alone.

The researchers say that the discovery could help doctors develop new drugs that block the communication pathway and treat pancreatic cancer. The study was published in Science Translational Medicine.

Pancreatic cancer cells spread by ‘educating’ the tumor environment

A team of researchers led by Dr. Michael S. Strickland from Memorial Sloan Kettering Cancer Center found evidence that pancreatic cancer cells communicate with the surrounding tissue via a protein called WNT5A. These interactions are necessary for the cancerous cells to thrive and grow into metastatic tumors.

The scientists used genetically engineered mouse models to show that blocking the interaction between WNT5A and its receptor Frizzled 2 slowed down the progression of the disease. They also showed that inhibiting the activity of WNT5A in human pancreatic cancer cell lines caused the same effect.

In addition, the researchers discovered that WNT5A levels increase during early stages of pancreatic cancer development. This suggests that targeting WNT5A could slow down the growth of the primary tumor.

Finally, the team analyzed data from over 300 patients diagnosed with pancreatic cancer and found that those whose tumors expressed high levels of WNT5A had shorter overall survival times compared to people whose tumors did not express this molecule.

GREM1 and pancreatic cancer

Researchers identified a protein associated with the spread of pancreatic cancers. They studied how this protein affects the transition of pancreatic cells from one form to another. They found that GREM1 promotes this change and increases the progression of PDAC.

They used mice and organoids—synthetic versions of human organs—to conduct their experiments. They wanted to see what role GREM1 played in the development of PDAC. To do this, they needed to understand how the protein affected cell growth.

The researchers grew organoids from normal mouse pancreas tissue and pancreatic cancer tissue. Then, they added GREM1 to some of the organoid cultures. Afterward, they compared the effect of GREM1 on the different types of tissues.

In addition to looking at the effects of GREM1 on cell growth, the scientists observed how the protein influenced the transition of pancreatic cancer cells from one stage to another. They saw that GREM1 promoted this process.

Study limitations and continued research

The findings published today are just one step toward finding a cure for pancreatic cancer. While the team discovered some interesting genetic differences among the different types of tumors, it still doesn’t explain why certain people develop pancreatic cancer while others don’t. In addition, this work does not provide any insight into whether these genetic alterations could be targeted therapeutically.

To address those questions, the researchers plan to continue studying human tissue samples. They hope to identify additional genes associated with pancreatic cancer and use those insights to help guide future studies.

Pancreatic cancer cells are ‘addicted’ to key protein

A study published in Nature Medicine suggests that it’s possible to identify a particular type of pancreatic cancer cell based on its unique genetic makeup. Researchers found that the most aggressive forms of pancreatic cancer rely on a key protein called PKM2 to help them grow and spread throughout the body.

The researchers used a technique known as CRISPR/Cas9 gene editing to alter the DNA of human pancreatic cancer cells. They discovered that altering the genes responsible for making PKM2 caused the cancer cells to die off. This finding could eventually lead to new treatments and preventative measures.

Finding out what drives tumor growth

Vakoc says his team found that a protein called ZEB1 was upregulated in most samples of pancreatic ductal adeno-carcinoma compared to normal pancreas. This protein binds to DNA, and its presence indicates that there are genes being turned off.

The researchers hypothesized that this particular protein could be responsible for making pancreatic ductal adenos-carcinoma so aggressive. They tested this idea by knocking down the expression of ZEB1 in human cell lines derived from pancreatic ductal adenes-carci-noma. When they did this, the cells became more like normal pancreas cells.

Suppressing P63 as a new treatment

The discovery could help scientists develop new ways to treat pancreatic cancer, one of the most deadly forms of the disease. Pancreatic cancer often spreads quickly throughout the body, making it difficult to detect early enough to cure.

To understand how the P63 gene became activated during the development of pancreatic cancers, researchers looked at human samples of both healthy pancreas and pancreatic tumors. They found that the gene was expressed in healthy tissues, but was turned off in the majority of pancreatic tumors.

In addition, they discovered that the gene was inactive in some healthy adult stem cells. But once those cells transformed into mature pancreatic cells, the gene was reactivated. This finding suggests that the gene might play a role in the transformation process.

To test whether suppressing the gene would stop cancer cell proliferation, the team analyzed several different types of pancreatic cancer cells grown in culture dishes. They found that inhibiting the gene caused the cells to die.

This study provides insight into how the gene works in vivo, says co-author Dr. Michael Wigler. He hopes that future research will uncover additional roles for the gene in pancreatic cancer progression.