Publications by authors named "Noelle Batista"

Article Synopsis
  • - Chromosome instability (CIN) is common in tumors, often driven by the breakage-fusion-bridge (BFB) cycle, but detailed mechanisms are still unclear.
  • - Researchers used a nuclease-dead Cas9 (dCas9) with a telomere-specific guide RNA to model the BFB cycle, finding that targeting telomeres causes DNA replication stress and increased DNA damage.
  • - The study revealed significant chromosome end fusions and other structures related to chromosome bridges, highlighting multiple DNA repair pathways involved in tumorigenesis and drug resistance.
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Chromosome instability (CIN) is frequently observed in many tumors. The breakage-fusion-bridge (BFB) cycle has been proposed to be one of the main drivers of CIN during tumorigenesis and tumor evolution. However, the detailed mechanisms for the individual steps of the BFB cycle warrants further investigation.

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Hutchinson-Gilford progeria syndrome (HGPS) is a rare, autosomal-dominant, and fatal premature aging syndrome. HGPS is most often derived from a de novo point mutation in the gene, which results in an alternative splicing defect and the generation of the mutant protein, progerin. Progerin behaves in a dominant-negative fashion, leading to a variety of cellular and molecular changes, including nuclear abnormalities, defective DNA damage response (DDR) and DNA repair, and accelerated telomere attrition.

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