In a ground breaking new study researchers have found that by inhibiting the action of a certain enzyme, known as TAK-1, it is possible to make pancreatic cancer cells more sensitive to chemotherapy treatments, paving the way to new and more effective treatments for the disease, which is currently considered incurable in most cases.
Dr Davide Melis, one of the study’s lead authors explained the significance of his teams work at a presentation before the ECCO 15 – ESMO 34 cancer conference in Berlin. “Pancreatic cancer is an incurable malignancy, resistant to every anti-cancer treatment. Targeting TAK-1 could be a strategy to revert this resistance, increasing the efficacy of chemotherapy,” he said. “During the past few years we have been studying the role played by a cytokine or regulatory protein called Transforming Growth Factor beta (TGFbeta) in the development of pancreatic cancer. Recently we focused our attention on a unique enzyme activated by TGFbeta, TAK-1, as a mediator for this extreme drug resistance.”
Dr Melis and his colleagues devoted their time to the study of the expression of TAK-1 in pancreatic cell lines and were able to develop a drug that specifically inhibited it. They then tested the action of both their TAK-1 inhibitor on its own and in conjunction with with various other commonly used anti cancer drugs such as gemcitabine, oxaliplatin and SN-38. Tests were performed both on established pancreatic cancer cell lines and in mice that had been genetically engineered with pancreatic cancer. In the mice they used only their TAK-1 inhibitor and the drug gemcitabine.
Their results were promising. According to Dr Melis by introducing the use of their TAK -1 inhibitor the researchers were able to use drug therapy that was 70 times lower than that used for a control group to kill the same number of cancer cells. In the mice they found that the tumor size was able to be significantly decreased, improving the animals’ lifespan.
Without the TAK-1 inhibitor gemcitabine.use by itself was highly ineffective because of the naturally drug resistant nature of the pancreatic cells. But once the Tak -1 inhibitor was added to the regime researchers saw a 78% reduction in tumor volumes, a significant result.
The main goal next for the research team is to begin transitioning their findings from the laboratory to the real life medical world. They are hoping to be able to begin clinical trails of their TAK-1 inhibitor in human pancreatic patients in the near future.