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David Scott

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Portland
As seen in: Associated Press, Medium, Nature, New York Post, PLOS ONE, MDPI, Taylor & Francis Online, BioRxiv, Cell Press, Healio, Orthopedics Today and
VP & Head of News Strategy and Operations, @AP.
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Articles

Regulatory factor X 7 limits Myc activity during B cell activation and suppresses Myc-dependent lymphomagenesis

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By Jessica Guerra, Maria Serena Merli, Pedro Ventura, Daniele Cavalli, Francesca Molinari, Andrea Rinaldi, Simone Moro, Ivo Kwee, Diego Morone, Simone Mosole, David Jarrossay, Luca Simonelli, Luca Varani, Egle Radice, Marcus Thelen, Clelia Di Serio, Margaret A. Shipp, Ryan D. Morin, David Scott Verified, Milo Frattini, Jessica Barizzi, Luciano Cascione, Francesco Bertoni, Davide F. Robbiani, Davide Rossi, Greta Guarda, Berenice A. Fischer, Hanif J. Khameneh, Alessandro Zenobi, Jasmine Ciorciari, Irene Buzzago, Alessandra Pfister, Lara Mattei, Chiara Montanino, Eleonora Calabretta, Kostantyn Dreval, Federico Jauk
| Nature Verified
Abstract Regulatory factor X 7 (RFX7) nonsense mutations have been found in different human B cell malignancies. We therefore set out to study the role of RFX7 in B cell activation and lymphomagenesis. Here we show that RFX7 truncations cause loss-of-function and dominant-negative effects. Moreover, low RFX7 mRNA levels correlate with worse diffuse large B cell lymphoma prognosis.
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Navigating Relational Complexity After Wilderness Accidents in Serious Leisure Contexts

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By Kelli McMahan, David Scott Verified
| Taylor & Francis Online
Advanced search Leisure Sciences An Interdisciplinary Journal Latest Articles Submit an article Journal homepage Full Article Figures & data References Citations Metrics Reprints & Permissions Read this article /doi/full/10.1080/01490400.2026.2670694?needAccess=true Abstract This study examined interpersonal strain and identity disruption following wilderness-based accidents among serious leisure participants.
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ZBTB11 depletion targets metabolic vulnerabilities in KRAS inhibitor-resistant PDAC - Nature Chemical Biology

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By Nathan L. Tran, Jiewei Jiang, Min Ma, Alyssa L. Verano, David Scott Verified, Eric Wang
| Nature Verified
Abstract Over 95% of pancreatic ductal adenocarcinomas (PDACs) harbor oncogenic mutations in KRAS. However, upon treatment with KRAS inhibitors, PDAC cells undergo rapid metabolic reprogramming toward an oxidative phosphorylation (OXPHOS)-dependent, drug-resistant state. Here, we demonstrate that this metabolic shift is associated with upregulation of the transcription factor ZBTB11 and both the metabolic state and resistance to KRAS inhibitors can be attenuated by ZBTB11 depletion.
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