Amanda Mitchell

ORCID: 0000-0003-4253-8717
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About
Contact & Profiles
Research Areas
  • Acute Myeloid Leukemia Research
  • Protein Degradation and Inhibitors
  • Epigenetics and DNA Methylation
  • Genetics and Neurodevelopmental Disorders
  • Histone Deacetylase Inhibitors Research
  • Ubiquitin and proteasome pathways
  • Cancer Genomics and Diagnostics
  • Immune cells in cancer
  • Intracerebral and Subarachnoid Hemorrhage Research
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Genomics and Chromatin Dynamics
  • Single-cell and spatial transcriptomics
  • Chronic Myeloid Leukemia Treatments
  • Acute Lymphoblastic Leukemia research
  • Sphingolipid Metabolism and Signaling
  • Hematopoietic Stem Cell Transplantation
  • Phagocytosis and Immune Regulation
  • RNA Interference and Gene Delivery
  • Cytokine Signaling Pathways and Interactions
  • Adipose Tissue and Metabolism
  • Acute Ischemic Stroke Management
  • MicroRNA in disease regulation
  • Autism Spectrum Disorder Research
  • RNA Research and Splicing
  • Digital Imaging for Blood Diseases

University Health Network
2016-2025

Health Net
2022-2025

Columbia University
2020-2024

Princess Margaret Cancer Centre
2015-2024

Columbia University Irving Medical Center
2024

National University Health System
2022

National University of Singapore
2022

UCLA Medical Center
2022

Icahn School of Medicine at Mount Sinai
2013-2022

Duke-NUS Medical School
2022

Highlights•Schizophrenia SNPs are enriched for eQTLs and cis-regulatory elements•The enrichment is greater enhancers in fetal adult brain tissue•Schizophrenia risk participate long-range promoter-enhancer interactions•CACNA1C variants associated with transcriptional regulation the brainSummaryA large portion of common variant loci genetic schizophrenia reside within noncoding sequence unknown function. Here, we demonstrate promoter enhancer expression quantitative trait (eQTL). The when...

10.1016/j.celrep.2014.10.015 article EN cc-by Cell Reports 2014-11-01

To investigate miRNA function in human acute myeloid leukemia (AML) stem cells (LSC), we generated a prognostic LSC-associated signature derived from functionally validated subpopulations of AML samples. For one miRNA, miR-126, high bioactivity aggregated all vivo patient sample LSC activity into single sorted population, tightly coupling miR-126 expression to function. Through functional studies, was found restrain cell cycle progression, prevent differentiation, and increase self-renewal...

10.1016/j.ccell.2015.12.011 article EN cc-by-nc-nd Cancer Cell 2016-01-28

Neuronal histone H3-lysine 4 methylation landscapes are defined by sharp peaks at gene promoters and other cis -regulatory sequences, but molecular cellular phenotypes after neuron-specific deletion of H3K4 methyl-regulators remain largely unexplored. We report that neuronal ablation the H3K4-specific methyltransferase, Kmt2a/Mixed-lineage leukemia 1 ( Mll1 ), in mouse postnatal forebrain adult prefrontal cortex (PFC) is associated with increased anxiety robust cognitive deficits without...

10.1523/jneurosci.3004-14.2015 article EN cc-by-nc-sa Journal of Neuroscience 2015-04-01

Cognitive abilities and disorders unique to humans are thought result from adaptively driven changes in brain transcriptomes, but little is known about the role of cis-regulatory affecting transcription start sites (TSS). Here, we mapped human, chimpanzee, macaque prefrontal cortex genome-wide distribution histone H3 trimethylated at lysine 4 (H3K4me3), an epigenetic mark sharply regulated TSS, identified 471 sequences with human-specific enrichment or depletion. Among these were 33 loci...

10.1371/journal.pbio.1001427 article EN cc-by PLoS Biology 2012-11-20

Cognitive defects in autism spectrum disorder (ASD) include socialization and communication: key behavioral capacities that separate humans from other species. Here, we analyze gene expression the prefrontal cortex of 63 patients control individuals, as well 62 chimpanzees macaques, natal to adult age. We show among all aberrant changes seen ASD brains, a single pattern overrepresented genes involved synaptic-related pathways is enriched nucleotide variants linked autism. Furthermore, only...

10.1371/journal.pbio.1002558 article EN public-domain PLoS Biology 2016-09-29

Therapy for acute myeloid leukemia (AML) involves intense cytotoxic treatment and yet approximately 70% of AML are refractory to initial therapy or eventually relapse. This is at least partially driven by the chemo-resistant nature leukemic stem cells (LSCs) that sustain disease, therefore novel anti-LSC therapies could decrease relapses improve survival. We performed in silico analysis highly prognostic human LSC gene expression signatures using existing datasets drug-gene interactions...

10.1038/s41408-018-0087-2 article EN cc-by Blood Cancer Journal 2018-06-06

Abstract Muscle regeneration depends on a robust albeit transient inflammatory response. Persistent inflammation is feature of age-related regenerative deficits, yet the underlying mechanisms are poorly understood. Here, we find inflammatory-related CC-chemokine-receptor 2 (Ccr2) expression in non-hematopoietic myogenic progenitors (MPs) during regeneration. After injury, Ccr2 MPs corresponds to levels its ligands, chemokines Ccl2, 7, and 8. We stimulation Ccr2-activity inhibits MP fusion...

10.1038/s41467-020-17620-8 article EN cc-by Nature Communications 2020-08-20

Abstract Acute myeloid leukemia (AML) is a caricature of normal hematopoiesis driven from stem cells (LSC) that share some hematopoietic cell (HSC) programs including responsiveness to inflammatory signaling. Although inflammation dysregulates mature and influences stemness lineage determination in HSCs by activating stress myelopoiesis, such roles LSCs are poorly understood. Here, we show S1PR3, receptor for the bioactive lipid sphingosine-1-phosphate, central regulator drives...

10.1158/2643-3230.bcd-20-0155 article EN Blood Cancer Discovery 2020-12-01
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