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Your search keyword '"Yu‐Wei Zhang"' showing total 3 results
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3 results on '"Yu‐Wei Zhang"'

1. HSCs: slow me down with PLAG1

Author

Yu Wei Zhang and Nina Cabezas-Wallscheid

Subjects
DNA-Binding Proteins, Immunology, Humans, Cell Biology, Hematology, Cell Self Renewal, Hematopoietic Stem Cells, Biochemistry, Transcription Factors
Published
2022

2. H3 K27M/I mutations promote context-dependent transformation in acute myeloid leukemia with RUNX1 alterations

Author

Vincent-Philippe Lavallée, Guy Sauvageau, Yu Wei Zhang, Elisa Tomellini, Bernhard Lehnertz, Nadine Mayotte, Josée Hébert, Isabel Boivin, and Jalila Chagraoui

Subjects
0301 basic medicine, Genetics, Mutation, Myeloid, Immunology, Myeloid leukemia, Context (language use), Cell Biology, Hematology, Biology, medicine.disease, medicine.disease_cause, Biochemistry, 03 medical and health sciences, Leukemia, chemistry.chemical_compound, Histone H3, 030104 developmental biology, medicine.anatomical_structure, RUNX1, chemistry, hemic and lymphatic diseases, medicine, Missense mutation
Abstract

Neomorphic missense mutations affecting crucial lysine residues in histone H3 genes significantly contribute to a variety of solid cancers. Despite the high prevalence of H3K27M mutations in pediatric glioblastoma and their well-established impact on global histone H3 lysine 27 di- and trimethylation (H3K27me2/3), the relevance of these mutations has not been studied in acute myeloid leukemia (AML). Here, we report the first identification of H3K27M and H3K27I mutations in patients with AML. We find that these lesions are major determinants of reduced H3K27me2/3 in these patients and that they are associated with common aberrations in the RUNX1 gene. We demonstrate that H3K27I/M mutations are strong disease accelerators in a RUNX1-RUNX1T1 AML mouse model, suggesting that H3K27me2/3 has an important and selective leukemia-suppressive activity in this genetic context.

Published
2017

3. H3K27M/I mutations promote context-dependent transformation in acute myeloid leukemia with RUNX1 alterations.

Author

Lehnertz, Bernhard, Yu Wei Zhang, Boivin, Isabel, Mayotte, Nadine, Tomellini, Elisa, Chagraoui, Jalila, Lavallée, Vincent-Philippe, Hébert, Josée, and Sauvageau, Guy

Subjects
*ACUTE myeloid leukemia, *GAIN-of-function mutations, *GLIOBLASTOMA multiforme, *LABORATORY mice, *HISTONES, *GENETICS
Abstract

Neomorphic missense mutations affecting crucial lysine residues in histone H3 cenes significantly contribute to a variety of solid cancers. Despite the high prevalence of H3K27M mutations in pediatric glioblastoma and their well-established impact on global histone H3 lysine 27 di- and trimethylation (H3K27me2/3), the relevance of these mutations has not been studied in acute myeloid leukemia (AML). Here, we repcrt the first identification of H3K2M and H3K27I mutations in patients with AML. We find thaLhese lesions are major determinants of reduced H3K27me2/3 in these patients and that they are associated with common aberrations in the RUNX1 gene. We demonstrate that H3K27I/M mutations are strong disease accelerators in a RUNX1-RUNX1T1 AML mouse model, suggesting that H3K27me2/3 has an important and selective leukemia-suppressive activity in this genetic context. [ABSTRACT FROM AUTHOR]

Published
2017
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