We are happy to present the results of our fruitful collaboration with researchers from University of Bern, Switzerland and from the Netherlands Cancer Institute. Zuzanna Nowicka and Wojciech Fendler MD PhD co-authored the article Functional Radiogenetic Profiling Implicates ERCC6L2 in Non-homologous End Joining in the August issue of Cell Reports.
In this study, genome-wide radiogenetic screen allowed to identify ERCC6L2, together with known DNA damage response genes and members of the shieldin and CTC1-STN1-TEN1 (CST) complexes, as a major determinant of cancer cell response to ionizing radiation. Such vulnerabilities in the DNA damage repair of cancer cells are an important area of investigation due to their crucial role in the development of therapeutic strategies that sensitize tumor to radiation.
ERCC6L2 loss was also shown here to restore DNA end resection and partially rescue homologus recombination in BRCA1 deficient cells, which was consistent with increased cellular radiosensitivity. Our team performed bioinformatic analysis to elucidate the importance of ERCC6L2 mutations in patients using publicly available data from The Cancer Genome Atlas (TCGA).