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Science Papers Describe CRISPR Alteration of T Cells for Cancer Patients, Sewage-Based Antimicrobial Resistance Surveillance, More

Cancer patients who received T cells engineered using the genome-editing technology CRISPR-Cas9 experienced no negative side effects from the treatment, according to a report in this week's Science. A team led by scientists from the University of Pennsylvania harvested T cells from three patients with refractory cancer, then used CRISPR-Cas9 to modify the cells in ways that improved their ability to target and fight tumors. When the modified T cells were reintroduced into the patients, they were found to persist for up to nine months with minimal immunogenicity. The results of this phase I study, the authors write, demonstrate the feasibility of CRISPR gene-editing for cancer immunotherapy. In a related editorial, University of California, Berkeley's Jennifer Doudna and Jennifer Hamilton discuss the trial results. The Scan also has more on this, here.

A global antimicrobial resistance (AMR) surveillance system based on the metagenomic sequencing of human sewage could represent an important addition to ongoing efforts to combat AMR, according to researchers from the Technical University of Denmark and the University of Edinburgh. In a policy piece in Science, the scientists note that such a surveillance approach is straightforward to implement, relatively cheap, and could characterize large populations without privacy concerns since data cannot be linked to any individual. Though not a substitute for other AMR surveillance methods, sewage-based surveillance "can provide data that is otherwise hard to obtain and may sometimes be the easiest route to providing any information at all, especially in resource-poor settings," they write. "By providing population-level information, it would complement and augment current AMR surveillance efforts, so contributing to meeting the key objectives of AMR surveillance at a global scale."

Two studies appearing in Science Translational Medicine this week provide new details about how a genetic risk factor for Alzheimer's disease and Parkinson's disease, the genotype APOE4, drives neurodegeneration and cognitive decline. In the first study, a Washington University team analyzed human and mouse data and found that animals expressing human APOE4 accumulated higher amounts of the Parkinson's disease market alpha-synuclein in the brainstem. These mice also showed poorer survival and more severe cognitive impairment than non-APOE4 mice. In humans, meanwhile, APOE4 was associated with rapid cognitive decline. In a second study, Mayo Clinic researchers found that mice expressing APOE4 had increased alpha-synuclein pathology, impaired behavioral performances, worsened neuronal and synaptic loss, and increased astrogliosis compared with animals with other APOE genotypes.