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New Therapy Brings Down Pancreatic Cancer Spread By 87%

If one is to make a list of the most difficult to treat types of cancer, pancreatic cancer would find itself in the top spot. That, however, may not be the case in the near future as scientists at the Albert Einstein College of Medicine have developed a new strategy, which brings down cancer metastases by around 87 percent. The findings of the study were published online in Science Translational Medicine.

As part of their study conducted on mice, researchers were able to make the pancreatic cells visible to the immune systems of the animals and thus vulnerable to immune attack. This brought down cancer metastases by 87 percent.

Commenting on the study findings, Claudia Gravekamp, corresponding author of the paper and a member of the National Cancer Institute-designated Albert Einstein Cancer Center, said, "Today's checkpoint inhibitor drugs work well against some types of cancer but only rarely help people with pancreatic cancer. The problem is that pancreatic tumors aren't sufficiently 'foreign' to attract the immune system's attention and can usually suppress whatever immune responses do occur. Essentially, our new therapy makes immunologically 'cold' tumors hot enough for the immune system to attack and destroy them."

The treatment strategy of the Albert Einstein Cancer Center researchers makes use of the fact that all people are vaccinated in childhood against tetanus, a serious disease caused by a toxic protein that Clostridium bacteria secrete. Thanks to their tetanus-specific memory T cells, which are present for lifelong in the bloodstream, vaccinated people will have strong immunity if they're ever again exposed to the highly foreign tetanus toxin. The researchers were able to successfully bring about a specific immune response against pancreatic cancer cells by injecting them with bacteria, which delivers tetanus toxin into the cells.

By making use of the very same tetanus vaccine given to humans, researchers vaccinated mouse models carrying human pancreatic tumors. They then joined together the gene, which codes for tetanus toxin into non-disease-causing Listeria monocytogenes bacteria, which are highly efficient at infecting cells and spreading through tissues. Lastly, to infect and "tetanize" the tumors, they inject the bacteria with their tetanus-gene cargoes into the previously vaccinated, tumor-bearing mice.

Once the Listeria bacteria affects the tumor cells, their tetanus-toxin genes expressed the tetanus-toxin protein inside the tumor cells, thus bringing about a strong immune response. The tetanus toxin makes active already existing tetanus-specific memory T cells, thus causing CD4 T cells to attack and kill the infected tumor cells.

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