The authors developed a refined gene expression signature (TRSS) that accurately measures replication stress independently of cell proliferation, addressing a major limitation of existing biomarkers that conflate stress with oncogene-driven growth. Applying this signature to patient samples, they discovered that replication stress is associated with activation of the non-homologous end-joining DNA repair pathway, suggesting cells may shift toward this repair mechanism under replication stress conditions.
Cell Stress (CES) emerges as a peer-reviewed publishing platform for high-impact research. CES publishes articles of extraordinary novelty and significance, including research papers and reviews that cover heterogenous topics in the field of cellular pathophysiology.
CES is an open access online journal that thus allows its readership and general public around the world to read, download, store, distribute or print any article free of charge. Long-term archiving and accessibility of all published articles is secured through partnership with different repositories, including PubMed Central.
At the same time, our open access policy ensures fast publication as well as high visibility and broad divulgence of the author’s published research. The financing of this policy is sustained by charging a publication fee/article processing charges (APCs). By pursuing an open access approach and the universal accessibility to scientific knowledge, we support the return to one of the essential values of science: the free exchange of ideas.
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