Associated Papers
Acute myeloid leukemia with concurrent NPM1 and RUNX1 mutations.
Zuo Z et al.
Leukemia Research Reports, 2023
Systematic Profiling of DNMT3A Variants Reveals Protein Instability Mediated by the DCAF8 E3 Ubiquitin Ligase Adaptor.
Huang YH et al.
Cancer Discovery, 2022
34429321 (PubMed )
Supplement: cd-21-0560_supplementary_table_1_suppst1.xlsx › Sheet1
Comprehensive germline and somatic genomic profiles of Chinese patients with biliary tract cancer.
Yu H et al.
Frontiers in Oncology, 2022
36072793 (PubMed )
Supplement: Table_2.xlsx › germline_alterations
Clonal evolution of acute myeloid leukemia revealed by high-throughput single-cell genomics.
Morita K et al.
Nature Communications, 2020
33087716 (PubMed )
Supplement: 41467_2020_19119_MOESM4_ESM.xlsx › Sheet1__2_
Next-Generation Sequencing Improves Diagnosis, Prognosis and Clinical Management of Myeloid Neoplasms.
Carbonell D et al.
Cancers, 2019
31540291 (PubMed )
Supplement: cancers-11-01364-s001.zip › cancers-588721-SI.pdf
Growth disrupting mutations in epigenetic regulatory molecules are associated with abnormalities of epigenetic aging.
Jeffries AR et al.
Genome Research, 2019
Identification of De Novo DNMT3A Mutations That Cause West Syndrome by Using Whole-Exome Sequencing.
Liu Z et al.
Molecular Neurobiology, 2018
The Tatton-Brown-Rahman Syndrome: A clinical study of 55 individuals with de novo constitutive DNMT3A variants.
Tatton-Brown K et al.
Wellcome Open Research, 2018
The spectrum of DNMT3A variants in Tatton-Brown-Rahman syndrome overlaps with that in hematologic malignancies.
Shen W et al.
American Journal of Medical Genetics. Part A, 2017
Mutations in Epigenetic Regulation Genes Are a Major Cause of Overgrowth with Intellectual Disability.
Tatton-Brown K et al.
American Journal of Human Genetics, 2017
28475857 (PubMed )
Supplement: mmc2.xlsx › Supplementary_Table_1
Mutations in the DNA methyltransferase gene DNMT3A cause an overgrowth syndrome with intellectual disability.
Tatton-Brown K et al.
Nature Genetics, 2014
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