Clinic I of Internal Medicine, University Hospital Cologne, Medical Faculty, University of Cologne, Cologne, 50937, Germany.
Published: March 2020
AI Article Synopsis
Article Abstract
The proximal DNA damage response kinase ATM is frequently inactivated in human malignancies. Germline mutations in the ATM gene cause Ataxia-telangiectasia (A-T), characterized by cerebellar ataxia and cancer predisposition. Whether ATM deficiency impacts on tumor initiation or also on the maintenance of the malignant state is unclear. Here, we show that Atm reactivation in initially Atm-deficient B- and T cell lymphomas induces tumor regression. We further find a reduced T cell abundance in B cell lymphomas from Atm-defective mice and A-T patients. Using T cell-specific Atm-knockout models, as well as allogeneic transplantation experiments, we pinpoint impaired immune surveillance as a contributor to cancer predisposition and development. Moreover, we demonstrate that Atm-deficient T cells display impaired proliferation capacity upon stimulation, due to replication stress. Altogether, our data indicate that T cell-specific restoration of ATM activity or allogeneic hematopoietic stem cell transplantation may prevent lymphomagenesis in A-T patients.
In this study, L. extracts were obtained using various green extraction techniques, including supercritical CO, subcritical ethanol, and ultrasound-assisted extraction, each performed under optimized parameters. The phytochemical content of the extracts was analyzed using the LC-MS/MS technique, quantifying 53 phytochemicals.
Background: Despite recurrent and activating mutations, including MYD88, CXCR4, ARID1A, KMT2D, and CD79B were identified, the genetic basis for Waldenström's Macroglobulinemia (WM) and the risk of progression of IgM MGUS to WM remain to be fully elucidated.
Methods: We investigated the mutation status of WM (n = 8), sWM (n = 7), and IgM MGUS (n = 5) patients, by performing high-throughput targeted AmpliSeq NGS on 117 target genes. Specifically, we analyzed the CD19+ cells from 15 WM/sWM patients and five IgM MGUS patients.
Titanium dioxide nanoparticles (TiO NPs) are among the most prevalent nanomaterials utilized in industrial and medical fields. However, their impact on spermatogenesis and male fertility remains insufficiently characterized. This study addresses the reproductive toxicity of TiO NPs and elucidates the underlying molecular mechanisms involved.
Introduction: The efficacy of radiotherapy in colorectal cancer (CRC) is often limited by radiation resistance. Ataxia telangiectasia mutated (ATM) is well known for its role in repairing double-strand DNA breaks within the DNA damage response (DDR) pathway. However, whether ATM mediates other mechanisms contributing to radiation resistance remains insufficiently investigated.
Recently, metal-based atomically thin materials (M-ATMs) have experienced rapid development due to their large specific surface areas, abundant electrochemically accessible sites, attractive surface chemistry, and strong in-plane chemical bonds. These characteristics make them highly desirable for energy-related conversion reactions. However, the insufficient active sites and slow reaction kinetics leading to unsatisfactory electrocatalytic performance limited their commercial application.
