ArticleProceedings of the National Academy of Sciences of the United States of America2025
G-quadruplex stabilization induces DNA breaks in pericentromeric repetitive DNA sequences in B lymphocytes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- BRIP1, a G-quadruplex DNA helicase, protects against AID-induced genomic instability by limiting R-loop accumulation.Molecular medicine (Cambridge, Mass.) · 2026Article
- G-quadruplex structures as regulators of cellular processes and drivers of genome instability in cancer.Critical reviews in biochemistry and molecular biology · 2026Review
- G-Quadruplexes: Structural Diversity and Emerging Roles in Biomolecular Condensation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
DNA secondary G-quadruplex (G4) structures can impair and even obstruct DNA replication. Defects in processing G4 structures are associated with replication stress, a common property of both B cell cancers and hyperproliferative premalignant cells. Genome instability arising from replication stress is a hallmark of cancer and strongly contributes to the chromosome rearrangements in B cell cancers. Here, we define the impact of G4-stabilizing ligands on generating genome instability in primary and malignant B cells. Treatment with the G4-stabilizing compound pyridostatin (PDS) causes breaks and chromosome rearrangements at ribosomal DNA and pericentromeric major satellite regions in both mouse primary B cell culture and CH12 lymphoma cells. PDS also causes extensive pericentromeric DNA damage in immortalized human B cell lines. Remarkably, PDS causes high level of tetraploid metaphase cells correlated with high level of dicentric chromosomes specifically in primary but not in CH12 B cells. Unlike primary B cells, CH12 cells undergo checkpoint activation and strong G2/M arrest in response to PDS treatment thus preventing tetraploid appearance. Altogether, these results highlight the difference between primary and malignant B cells in response to PDS, revealing the therapeutic potential of G4-stabilizing drugs to selectively suppress tumor cell growth and proliferation.
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