A
Antonio Sarno
Researcher at Norwegian University of Science and Technology
Publications - 36
Citations - 1120
Antonio Sarno is an academic researcher from Norwegian University of Science and Technology. The author has contributed to research in topics: DNA glycosylase & DNA repair. The author has an hindex of 13, co-authored 27 publications receiving 787 citations. Previous affiliations of Antonio Sarno include SINTEF & Central Norway Regional Health Authority.
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Detailed analysis of p53 pathway defects in fludarabine-refractory chronic lymphocytic leukemia (CLL): dissecting the contribution of 17p deletion, TP53 mutation, p53-p21 dysfunction, and miR34a in a prospective clinical trial.
Thorsten Zenz,Sonja Häbe,Tina Denzel,Julia Mohr,Dirk Winkler,Andreas Bühler,Antonio Sarno,Silja Groner,Daniel Mertens,Raymonde Busch,Michael Hallek,Hartmut Döhner,Stephan Stilgenbauer +12 more
TL;DR: Although TP53 mutations and 17p deletions are found in a high proportion of F-refractory CLL, more than half of the cases cannot be explained by p53 defects (deletion or mutation), and alternative mechanisms need to be investigated.
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Small-molecule inhibitor of OGG1 suppresses proinflammatory gene expression and inflammation.
Torkild Visnes,Torkild Visnes,Armando Cázares-Körner,Wenjing Hao,Olov A. Wallner,Geoffrey Masuyer,Olga Loseva,Oliver Mortusewicz,Elisee Wiita,Antonio Sarno,Aleksandr Manoilov,Juan Astorga-Wells,Ann-Sofie Jemth,Lang Pan,Kumar Sanjiv,Stella Karsten,Camilla Göktürk,Maurice Grube,Evert Homan,Bishoy M. F. Hanna,Cynthia B.J. Paulin,Therese Pham,Azita Rasti,Ulrika Warpman Berglund,Catharina Von Nicolai,Carlos Benitez-Buelga,Tobias Koolmeister,Dag Ivanic,Petar Iliev,Martin Scobie,Hans E. Krokan,Pawel Baranczewski,Pawel Baranczewski,Pawel Baranczewski,Per Artursson,Per Artursson,Mikael Altun,Annika Jenmalm Jensen,Christina Kalderén,Xueqing Ba,Roman A. Zubarev,Roman A. Zubarev,Pål Stenmark,Pål Stenmark,Istvan Boldogh,Thomas Helleday,Thomas Helleday +46 more
TL;DR: A small-molecule drug that acts as a potent and selective active-site inhibitor that stops OGG1 from recognizing its DNA substrate and hampers Ogg1 binding to and repair of 8-oxoG is developed, which is well tolerated by mice and presents a proof of concept that targeting oxidative DNA repair can alleviate inflammatory conditions in vivo.
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UV degradation of natural and synthetic microfibers causes fragmentation and release of polymer degradation products and chemical additives
Lisbet Sørensen,Anette Synnøve Groven,Ingrid Alver Hovsbakken,Oihane Del Puerto,Daniel Franklin Krause,Antonio Sarno,Andy M. Booth +6 more
TL;DR: A range of molecular degradation products were identified in seawater leachates after UV exposure, with increasing abundance over the duration of the experiment, and a variety of additive chemicals were shown to leach from the MFs into seawater.
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AID expression in B-cell lymphomas causes accumulation of genomic uracil and a distinct AID mutational signature.
Henrik Sahlin Pettersen,Anastasia Galashevskaya,Berit Doseth,Mirta M. L. Sousa,Antonio Sarno,Torkild Visnes,Per Arne Aas,Nina-Beate Liabakk,Geir Slupphaug,Pål Sætrom,Bodil Kavli,Hans E. Krokan +11 more
TL;DR: Evidence from mass spectrometric quantitation of deoxyuridine in DNA that shows significantly higher genomic uracil content in B-cell lymphoma cell lines compared to non-lymphoma cancer cell lines and normal circulating lymphocytes is presented, indicating that AID-induced mutagenic U:G mismatches in DNA may be a fundamental and common cause of mutations inB-cell malignancies.
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Modulation of cell metabolic pathways and oxidative stress signaling contribute to acquired melphalan resistance in multiple myeloma cells
Kamila Anna Zub,Mirta M. L. Sousa,Antonio Sarno,Animesh Sharma,Aida Demirovic,Shalini V. Rao,Clifford Young,Per Arne Aas,Ida Ericsson,Anders Sundan,Ole N. Jensen,Geir Slupphaug +11 more
TL;DR: Changes in cellular processes and pathways not previously associated with melphalan resistance in multiple myeloma cells are discovered, including a metabolic switch conforming to the Warburg effect (aerobic glycolysis), and an elevated oxidative stress response mediated by VEGF/IL8-signaling.