Nat Commun: New potential anti-cancer therapies may effectively enhance the immune response of host bodies to target cancer treatments

11, 2020 // -- In a recent study published in the international journal Nature Communications, scientists from Siddasenai Medical Center and others developed a new approach to cancer therapy by studying cancer cells in humans and mice and laboratory mice, possible by transforming the commonly used chemotherapy drug Gissytabin into a drug that kills cancer cells in a special way, thereby activating host immune cells to fight cancer.
researchers say that when they added the FDA-approved anti-inflammatory drug Celebrex to the Gissetham chemotherapy method, it could turn Gissythabin, a non-immunogenic drug that does not activate the patient's autoimmune response, into an immunogenic drug that induces an immune response in mice.
combination of drugs or can achieve the "one arrow, two carvings" purpose, that is, both to kill tumor cells and activate the host body's immune cells. 'I think the results of this study have significant clinical potential because cancer immunotherapy is now an important pillar in the treatment of cancer patients, and if this finding is clinically proven, it could potentially increase the proportion of patients who respond to cancer immunotherapy in the future,' said chan,
researcher.
file photo: CC0 Public Domain Currently, about 70 to 85 percent of patients taking immunotherapy drugs do not respond to the treatment; since the 1940s, the main treatment for killing cancer cells has been chemotherapy drugs, which can kill cancer cells directly.
But many drugs may not be able to induce the most effective form of cell death, immunogenic cell death, which activates the release of a protein called a "de" or "dangerous" signal that promotes what is called Instead of stimulating T-cells to remove tumors, most chemotherapy currently treats pancreatic, bladder, breast, ovarian and non-small cell lung cancers is not just non-immunogenic because it inhibits the function of the host body's immune system.
In recent years, immunotherapy drugs have often been added to chemotherapy programmes or used alone to help patients attack cancer with their own immune cells, but patients tend to respond less; In the
study, the researchers found that while Gissithamin does release a "go" signal, it also promotes the release of an inhibitory signal that blocks the function of dedescant cells to activate the killing of cancer T cells, which would not reach anywhere if the inhibitory signal was turned on, making it necessary for researchers to find a balance between the "go" signal and the brake signal to promote a more effective immune response.
researchers found that the way to balance this balance was the anti-inflammatory drug celexib, which removes inhibitory signals to leave only a "go" signal, and then the tyrobladge and T cells were better able to perform their immune response in the host body, while gisitapons could also be converted into immunogenic drugs.
researcher Hayashi said that by focusing more the accelerator to release the go signal, we were able to remove the pedals that blocked the brakes, allowing dendrites to induce T-cells to kill tumors.
researchers believe that adding immunotherapy drugs to the therapeutic strategies of Gisithamin and Celexib may make the host's immune response perform better, and are now testing the hypothesis that they expect more studies later to test the efficacy of new therapies in randomized, placebo-controlled trials.
Finally, researchers say that using the patient's own immune system to attack a patient's tumor cells may be an important tool to help treat cancer, and unfortunately, researchers have failed in many patients so far, and this study may reveal a potential mechanism to explain why these patients failed to treat, potentially offering a potentially new solution.
() Original source: Hayashi, K., Nikolos, F., Lee, Y.C. et al. Tipping the immunostimulatory and inhibitory DAMP balance to harness immunogenic cell death. Nat Commun 11, 6299 (2020). doi:10.1038/s41467-020-19970-9。