DDX54 downregulation enhances anti-PD1 therapy in immune-desert lung tumors with high tumor mutational burden
The twenty-one courses on this site were built, in order, to make this one paper readable. A high mutational burden (TMB-H) is supposed to predict that immunotherapy will work — yet a large share of lung tumours stay 'immune deserts' that T cells never enter. Kwang-Hyun Cho's group at KAIST traced that to a single master regulator, DDX54, and showed that turning it down makes previously useless anti-PD1 therapy start working. Public-data analysis, network simulation, molecular mechanism and mouse experiments all live inside this one article — the whole arc of bioinformatics in a single read. That is why it is this week's paper.
This paper's licence (CC BY-NC-ND 4.0) does not permit public distribution of derivative works. The Korean, high-school and executive editions live inside the signed-in classroom only.