Genomic instability, DNA replication and Recombination (Campbell Lab)

Cancer cells are undergoing replication stress due to oncogene activation or ablation of tumor suppression. Recent studies point to stalled replication forks as major culprit in generating mutation and genome rearrangement that correlate with tumor progression. The aim of our studies is to understand events at stalled DNA replication forks. Projects range from delineation of the delicate balance of remodeling, degradation and restart at stalled replication forks involving helicases and nucleases to characterization of small molecule inhibitors of one of the major players in replication fork stability. These inhibitors have applications in killing replication stressed tumor cells, in sensitizing tumor cells to chemotherapies and radiation therapies that interfere with replication fork progression, and synergizing with other DNA repair inhibitors in combinatorial therapies. A background in the DNA damage response, repair, recombination, and/or DNA replication is preferred but not essential.

Candidates with a record of publication in peer–reviewed journals and expertise in human cell culture, shRNA and siRNA knockdowns, IPs, westerns, cell line derivation, standard molecular biological techniques and cell biological techniques (e.g. immunfluorescence, cell cycle, and chromosome analysis) are sought. Experience with pulse-labeling of DNA, DNA fiber tracking, protein expression and/or purification, in vitro assays of enzymes of DNA metabolism, mouse xenograft experiments, and/or bioinformatics is preferred but not required.

To apply: Please send a detailed curriculum vitae, a short statement on future research goals, and names and contact details for three references, including your PhD supervisor, to Prof. Campbell at

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