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Homo sapiens

ABSTRACT: The DNA Double-Strand Break Response Is Abnormal in Myeloblasts From Patients With Therapy-Related Acute Myeloid Leukemia [NimbleGen]

OTHER RELATED OMICS DATASETS IN: E-GEOD-52478GSE53251

PROVIDER: PRJNA231541 | ENA |

REPOSITORIES: ENA

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E-GEOD-52478

Project description:The DNA Double-Strand Break Response Is Abnormal in Myeloblasts From Patients With Therapy-Related Acute Myeloid Leukemia

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Elevated dNTP Pool Levels Impair Homologous Recombination and Enhance Glioblastoma Sensitivity to Irradiation and Temozolomide

Project description:Glioblastoma (GBM) standard of care includes surgical resection followed by ionizing radiation (IR) and Temozolomide, which induce DNA double-strand breaks. Homologous recombination (HR), a critical DNA double-strand break repair pathway, is augmented in GBM, contributing to resistance and poor patient outcomes. Here, we demonstrate that increasing dNTP levels impairs HR-mediated double-strand break repair, rendering GBM cells sensitive to IR and Temozolomide. Interestingly, combining an elevated dNTP pool level with IR and/or Temozolomide promotes the recruitment of DNA polymer-ase-α/primase, which is typically involved in Okazaki fragment synthesis during DNA replication, to the DNA double-strand break site, thereby interfering with DNA end resection. Specifically, higher dNTP pool levels disrupted the recruitment of HR-associated proteins such as RPA70 and RAD51, an effect reversed by Aphidicolin, a DNA polymerase-α/primase inhibitor. Impaired HR delayed IR- and/or Te-mozolomide-induced DNA double-strand break repair, leading to growth arrest and apoptosis. Furthermore, higher dNTP pool levels led to downregulation of DNA repli-cation and HR-associated genes, while upregulating several pro-apoptotic genes. In-creased sensitivity to IR and Temozolomide was also observed in engineered IR-resistant GBM cell lines and in naturally recurrent patient-derived GBM cells that emerge post-therapy. These findings emphasize how dNTP pool levels regulate HR and uncover a promising vulnerability that could be exploited to overcome resistance to DNA-damaging treatments in GBM and beyond.

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