Whereas ATM signaling is well known to be activated by DNA doubles-strand breaks, this study provides new evidence that ATM signaling is directly activated by DNA single-strand breaks and activated and regulated by APE1 in eukaryotic systems.
Tag: DNA Damage Response
MD Anderson Research Highlights for February 21, 2024
The University of Texas MD Anderson Cancer Center’s Research Highlights showcases the latest breakthroughs in cancer care, research and prevention. These advances are made possible through seamless collaboration between MD Anderson’s world-leading clinicians and scientists, bringing discoveries from the lab to the clinic and back. Recent developments at MD Anderson offer insights into drug-drug interactions for patients with acute myeloid leukemia (AML) and myelodysplastic syndromes; patient-derived xenograft models as a viable translational research tool in early-phase clinical trials; a novel gene expression signature to stratify patients with bladder cancer; a potential therapeutic target to overcome treatment resistance in multiple myeloma; a role for mutant p53 in protecting against ferroptosis in triple-negative breast cancer; and diet modifications to improve treatment outcomes in FLT3-mutated AML.
MD Anderson Research Highlights for June 7, 2023
The University of Texas MD Anderson Cancer Center’s Research Highlights showcases the latest breakthroughs in cancer care, research and prevention.
Motion of DNA linked to its damage response, ability to repair itself
Indiana University researchers have discovered that the motion of chromatin, the material that DNA is made of, can help facilitate effective repair of DNA damage in the human nucleus — a finding that could lead to improved cancer diagnosis and treatment.
Troublemaking ‘lesion’ singled out in UV-caused skin cancer
Upon exposure to human skin, ultraviolet light from the sun almost instantly generates two types of “lesions” that damage DNA. Scientists at UW Medicine in Seattle determined which of these lesions is responsible for activating a process that may increase cancerous mutations in cells.