Pancreatic cancer is currently proving to be a challenge in terms of treatment as only 8% of the patients have been found to survive after the diagnosis. As the chemotherapy and radiation therapy have limited benefit, the doctors have now shifted to immunotherapy which is believed to have revolutionized treatment for distant kinds of cancer by stimulating the body’s immune system to combat cancer cells. The researchers from the Washington University School of Medicine and Rush University have found a chemical compound that activates a strong immune attack against lethal cancer. The new compound can reduce tumor growth and metastases in mice models. The shrinking of the tumors helped improve the survival rate in the animals.
The immune-accelerating compound can turn resistant pancreatic cancers into susceptible ones that can easily be targeted by immunotherapy. The lethal disease is in desperate need for new therapeutic approaches. The compound helps by releasing the brakes put on the T cells so as to start attacking the cancer cells. The use of immunotherapies in pancreatic cancer improved the lives of only 5% of the patients. Instead of the T cells, the researchers have now shifted their focus on the myeloid cells that are generally found circling the tumors. The myeloid cells in pancreatic cancer tend to suppress the T cells and other immune cells and in turn, reduce the effectiveness of immunotherapy.
Other than removing the brakes o T cells, reducing myeloid cells and in turn activating T cells to attack is important. The chemical compound ADH-503 is found to interfere with the migration of myeloid cells. This compound helped drop the number of myeloid cells that in turn boosted the immune responses. Boston Biomedical has recently decided to stop a late-stage trial of its experimental drug along with previous chemotherapies after it botched to treat pancreatic cancer patients. The traditional cancer chemo agents Abraxane and gemcitabine were combined with Boston Biomedical’s investigational oncology drug napabucasin, which is an oral therapy stimulated by NQO1 and it is expected to result in the death of cancer cells.