R
Roberto Tapia
Researcher at Washington University in St. Louis
Publications - 3
Citations - 121
Roberto Tapia is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Haematopoiesis & Gene mutation. The author has an hindex of 3, co-authored 3 publications receiving 91 citations.
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Mutant U2AF1-expressing cells are sensitive to pharmacological modulation of the spliceosome
Cara Lunn Shirai,Brian S. White,Manorama Tripathi,Roberto Tapia,James N Ley,Matthew Ndonwi,Sang-hyun Kim,Jin Shao,Alexa Carver,Borja Saez,Robert S. Fulton,Catrina Fronick,Michelle O'Laughlin,Chandraiah Lagisetti,Thomas R. Webb,Timothy A. Graubert,Matthew J. Walter +16 more
TL;DR: It is found that haematopoietic cells expressing mutant U2AF1(S34F), including primary patient cells, have an increased sensitivity to in vitro sudemycin treatment relative to controls, suggesting a potential for treating haem atological cancers harbouring U2 AF1 mutations with pre-mRNA splicing modulators like sudemies.
Journal ArticleDOI
c-Myb and C/EBPβ regulate OPN and other senescence-associated secretory phenotype factors.
Kevin C. Flanagan,Elise Alspach,Ermira Pazolli,Shankar Parajuli,Qihao Ren,Laura L. Arthur,Roberto Tapia,Sheila A. Stewart +7 more
TL;DR: The transcription factor c-Myb regulates OPN, IL-6, and IL-8 in addition to 57 other SASP factors, and the depletion of either factor reduces the ability of senescent fibroblasts to promote the growth of preneoplastic epithelial cells.
Journal ArticleDOI
Preclinical Activity of Splicing Modulators in U2AF1 Mutant MDS/AML
Cara Lunn Shirai,Manorama Tripathi,James N Ley,Matthew Ndonwi,Brian S. White,Roberto Tapia,Borja Saez,Amy M. Bertino,Jin Shao,Sang-hyun Kim,Thomas R. Webb,Timothy A. Graubert,Matthew J. Walter +12 more
TL;DR: It is hypothesized that cells harboring spliceosome gene mutations have increased sensitivity to pharmacological perturbation of the splicingosome by splicing modulator drugs, providing a new treatment approach for patients with U2AF1 mutations.