ArticleNAR cancer2026
Disruption of the structural maintenance of chromosomes 5/6 complex enables tumor mutagenesis.
Article in NAR cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- The Multifunctional SMC5/6 Complex in Genome Stability, Antiviral Restriction, and Human Disease.Current issues in molecular biology · 2026Review
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4 authors.
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Abstract
The structural maintenance of chromosomes (SMC) 5/6 complex is conserved and essential for mammalian development. SMC5/6 germline variants in cells, model organisms, and patients results in genome instability. However, the consequences of somatic SMC5/6 dysfunction in cancer are unknown. We report a pan-cancer analysis of SMC5/6 variants across three databases in which thousands of tumors across all tissue types harbored copy number alteration (CNA) and/or small variants in SMC5/6 genes. We found that deleterious variants-those predicted to cause protein disruption, but not CNAs, in SMC5/6 genes were associated with elevated tumor mutational burden (TMB). Mutagenesis in tumors with deleterious SMC5/6 variants was largely due to polymerase epsilon dysfunction and mismatch repair deficiency. Patients with SMC5/6 gene variants in tumors exhibited improved survival, in part due to a superior response to immunotherapy. Our findings demonstrate that SMC5/6 complex disruption in cancer predicts elevated TMB and susceptibility to immunotherapy, indicating the potential to use SMC5/6 gene status for prognostic implications and tailored therapeutic approaches.
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