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Both episode checkpoint inhibitors and adoptive cell therapy are novel immunotherapies that have the potential to treat solid tumors such as HBV-associated hepatocellular carcinoma (HCC), however, they all have their own drawbacks.
For a very long time, it has been thought that the neurodegenerative disorder of Alzheimer's disease is caused by β-amyloid plaques, which is called Amyloid Precursor Protein (APP), breaking down into fragments and accumulates in the brain to form misfolded, toxic polymers that impede neural communication. In the presence of Alzheimer's disease, β-amyloid plaques will lead to neuronal death directly, or destroy the nutritional supply of brain cells through the action of tau protein phosphorylation (tau protein bending to form neurofibrillary tangles), eventually killing them. However, a new study recently published in Stem Cell Reports by the University of Queensland, Australia suggested that we may need to rethink the biological mechanisms that lead to cognitive decline in Alzheimer's disease.
Recently, researchers at Northwestern University Medical School successfully prevented the growth of glioblastoma which was an invasive form of brain cancer by inhibiting an enzyme called CDK5. The related study has been published in the Journal of Cell Reports.
Recently, researchers from the Hollings Cancer Center at the University of Southern Carolina Medical School (MUSC) discovered that tumor cells use unfolded protein response (UPR) to change the biological clock, which further leads to tumor growth as a key part of the biological clock precisely inhibits the tumor growth process. Related study results being published in the Nature Cell Biology.
