Ottawa scientists to fight silent killer of #PancreaticCancer with viruses?


One of Ottawa’s premier research scientists has published a study that points to viruses as an important ally in the fight against pancreatic cancer, a disease known as a “silent killer” because its early symptoms often go unnoticed.

People diagnosed with pancreatic cancer have a five-year survival rate of just six per cent. That survival rate — the lowest among all common cancer types — has not improved in the past four decades.

Major surgery remains the only way of curing pancreatic cancer, but it’s usually performed only if the tumour has not spread beyond the organ. In most cases (85 per cent), the cancer is not detected early enough to make surgery viable.

Pancreatic cancer is also resistant to conventional treatments, such as chemotherapy and radiation, because of the unusual architecture of the tumours, which have a heavy concentration of stromal cells. The cells interact with pancreatic cancer cells, protect the tumour, and promote its growth.

In a study released Monday, however, Ottawa researchers say that the same biology that makes pancreatic tumours so robust also makes them vulnerable to attack by engineered viruses.

“The reason we’re so excited about these viruses is that they take advantage of the same things that the tumour uses to become a really good tumour: They exploit those for therapeutic benefit,” said Dr. John Bell, an Ottawa Hospital Research Institute senior scientist, who co-authored the study with post-doctoral fellow, Dr. Carolina Ilkow, and others.

Published in Nature Medicine, the study describes experiments designed to better understand the “ecosystem” of pancreatic tumours, which include complex networks of stromal and malignant cells. Stromal cells normally help maintain tissue, but can be co-opted by cancer cells to promote tumour growth.

Researchers isolated the cell types and studied them, then studied how they interacted with each other and with viruses. Much to their surprise, they discovered that the interaction between stromal and malignant cells made them more vulnerable to viral infection.

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