Beisi Xu

ORCID: 0000-0003-0099-858X
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About
Contact & Profiles
Research Areas
  • Neuroblastoma Research and Treatments
  • Epigenetics and DNA Methylation
  • Genomics and Chromatin Dynamics
  • Acute Myeloid Leukemia Research
  • RNA modifications and cancer
  • interferon and immune responses
  • Immune Cell Function and Interaction
  • Protein Degradation and Inhibitors
  • Acute Lymphoblastic Leukemia research
  • T-cell and B-cell Immunology
  • RNA Research and Splicing
  • Retinal Development and Disorders
  • Cytokine Signaling Pathways and Interactions
  • Chromatin Remodeling and Cancer
  • Immune cells in cancer
  • Cancer-related molecular mechanisms research
  • RNA and protein synthesis mechanisms
  • Ubiquitin and proteasome pathways
  • Genomics and Rare Diseases
  • CAR-T cell therapy research
  • Cancer Genomics and Diagnostics
  • CRISPR and Genetic Engineering
  • Cancer-related gene regulation
  • Glioma Diagnosis and Treatment
  • Immunotherapy and Immune Responses

St. Jude Children's Research Hospital
2016-2025

Children's Research Hospital
2020

Children's Hospital
2019

City of Hope
2011-2015

Beckman Research Institute
2011-2015

Dalian Institute of Chemical Physics
2011-2013

Chinese Academy of Sciences
2011-2013

University of Tennessee Health Science Center
2013

University of Science and Technology of China
2004-2009

Indiana University – Purdue University Indianapolis
2009

The amplified MYCN gene serves as an oncogenic driver in approximately 20% of high-risk pediatric neuroblastomas. Here, we show that the family member MYC is a potent transforming separate subset neuroblastoma cases (∼10%), based on (i) its upregulation by focal enhancer amplification or genomic rearrangements leading to hijacking, and (ii) ability transform precursor cells transgenic animal model. aberrant regulatory elements associated with activation include focally distal enhancers...

10.1158/2159-8290.cd-17-0993 article EN Cancer Discovery 2017-12-29

Lineage-ambiguous leukemias are high-risk malignancies of poorly understood genetic basis. Here, we describe a distinct subgroup acute leukemia with expression myeloid, T lymphoid, and stem cell markers driven by aberrant allele-specific deregulation BCL11B, master transcription factor responsible for thymic T-lineage commitment specification. Mechanistically, this was chromosomal rearrangements that juxtapose BCL11B to superenhancers active in hematopoietic progenitors, or focal...

10.1158/2159-8290.cd-21-0145 article EN Cancer Discovery 2021-06-08

Numerous pieces of evidence support the complex, 3D spatial organization genome dictates gene expression. CTCF is essential to define topologically associated domain boundaries and facilitate formation insulated chromatin loop structures. To understand CTCF's direct role in global transcriptional regulation, we integrated miniAID-mClover3 cassette endogenous locus a human pediatric B-ALL cell line, SEM, an immortal erythroid precursor HUDEP-2, allow for acute depletion protein by...

10.1093/nar/gkz462 article EN cc-by Nucleic Acids Research 2019-05-15

Abstract Aggressive cancers often have activating mutations in growth-controlling oncogenes and inactivating tumor-suppressor genes. In neuroblastoma, amplification of the MYCN oncogene inactivation ATRX gene correlate with high-risk disease poor prognosis. Here we show that are mutually exclusive across all ages stages neuroblastoma. Using human cell lines mouse models, found elevated expression incompatible. Elevated levels promote metabolic reprogramming, mitochondrial dysfunction,...

10.1038/s41467-020-14682-6 article EN cc-by Nature Communications 2020-02-14

Abstract UBTF tandem duplications (UBTF-TDs) have recently emerged as a recurrent alteration in pediatric and adult acute myeloid leukemia (AML). UBTF-TD leukemias are characterized by poor response to conventional chemotherapy transcriptional signature that mirrors NUP98-rearranged NPM1-mutant AMLs, including HOX-gene dysregulation. However, the mechanism which drives leukemogenesis remains unknown. In this study, we investigated genomic occupancy of transformed cord blood CD34+ cells...

10.1182/blood.2023021359 article EN cc-by-nc-nd Blood 2023-10-27

Abstract Standard normal mode analysis (NMA) method is able to calculate vibrational entropy of proteins, but it computationally intensive, especially for large proteins. To evaluate efficiently and accurately, we, here, propose computation schemes based on coarse‐grained NMA methods. This can be achieved by rescaling results with a specific factor that derived the basis linear correlation protein between standard NMA. Our repeat correctly © 2011 Wiley Periodicals, Inc. J Comput Chem,

10.1002/jcc.21900 article EN Journal of Computational Chemistry 2011-08-27

Abstract Background DNA methylation patterns are initiated by de novo methyltransferases DNMT3a/3b adding methyl groups to CG dinucleotides in the hypomethylated genome of early embryos. These faithfully maintained DNMT1 during replication ensure epigenetic inheritance across generations. However, this two-step model is based on limited data. Results We generated base-resolution methylomes for a series DNMT knockout embryonic stem cells, with deep coverage at highly repetitive elements. show...

10.1186/s13059-015-0685-2 article EN cc-by Genome Biology 2015-06-01

Glioblastoma (GBM) is an immunologically "cold" tumor that does not respond to current immunotherapy. Here, we demonstrate a fundamental role for the α-isoform of catalytic subunit protein phosphatase-2A (PP2Ac) in regulating glioma immunogenicity. Genetic ablation PP2Ac cells enhanced double-stranded DNA (dsDNA) production and cGAS-type I IFN signaling, MHC-I expression, mutational burden. In coculture experiments, deficiency promoted dendritic cell (DC) cross-presentation clonal expansion...

10.1158/0008-5472.can-22-3382 article EN Cancer Research 2023-05-23
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