Publications by authors named "R E SCULLY"

Tandem duplications (TD) are among the most frequent type of structural variant (SV) in the cancer genome. They are characterized by a single breakpoint junction that defines the boundaries and the size of the duplicated segment. Cancer-associated TDs often increase oncogene copy number or disrupt tumor suppressor gene function, and thus have important roles in tumor evolution.

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Replication fork collision with a DNA nick can generate a one-ended break, fostering genomic instability. The opposing fork's collision with the nick could form a second DNA end, enabling conservative repair by homologous recombination (HR). To study mechanisms of nickase-induced HR, we developed the Flp recombinase "step arrest" nickase in mammalian cells.

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Context: Ireland has one of the most rural populations in Europe. Rurality presents challenges when accessing health services but should not be perceived as problematic and in need of a structural fix. Structural urbanism where health care is viewed as a commodity for individuals, rather than an infrastructure for populations, innately favours larger urban populations and has detrimental outcomes for rural health.

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Article Synopsis
  • Replisome collisions with damaged DNA can cause double strand breaks (DSBs) that impact cancer development and treatment.
  • Recent studies indicate these collisions can result in either single-ended or double-ended DSBs, each influencing repair methods and the risk of genomic instability differently.
  • There is new evidence that the conditions around broken DNA replication sites in mammals may favor a repair process called homologous recombination over another process known as non-homologous end joining.
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Collision of a replication fork with a DNA nick is thought to generate a one-ended break, fostering genomic instability. Collision of the opposing converging fork with the nick could, in principle, form a second DNA end, enabling conservative repair by homologous recombination (HR). To study mechanisms of nickase-induced HR, we developed the Flp recombinase "step arrest" nickase in mammalian cells.

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