Emily Heikamp

ORCID: 0000-0002-4591-4477
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About
Contact & Profiles
Research Areas
  • Marriage and Sexual Relationships
  • T-cell and B-cell Immunology
  • Epigenetics and DNA Methylation
  • Acute Myeloid Leukemia Research
  • Protein Degradation and Inhibitors
  • Immune Cell Function and Interaction
  • Angiogenesis and VEGF in Cancer
  • Histone Deacetylase Inhibitors Research
  • PI3K/AKT/mTOR signaling in cancer
  • Childhood Cancer Survivors' Quality of Life
  • Acute Lymphoblastic Leukemia research
  • Kruppel-like factors research
  • Genomics and Chromatin Dynamics
  • Brain Metastases and Treatment
  • Mast cells and histamine
  • Congenital heart defects research
  • Neonatal Respiratory Health Research
  • RNA modifications and cancer
  • Monoclonal and Polyclonal Antibodies Research
  • Child and Adolescent Health
  • Cancer Immunotherapy and Biomarkers
  • Pediatric Pain Management Techniques
  • Blood disorders and treatments
  • Emergency and Acute Care Studies
  • Multiple Myeloma Research and Treatments

Dana-Farber Cancer Institute
2019-2024

Boston Children's Hospital
2021-2024

Harvard University
2021-2024

Michigan United
2023

Shaare Zedek Medical Center
2023

Children's Hospital at Montefiore
2023

Albert Einstein College of Medicine
2023

Rainbow Babies & Children's Hospital
2023

Northwestern University
2023

Zhejiang University
2023

Tumors build vessels by cooption of pre-existing vasculature and de novo recruitment bone marrow (BM)-derived endothelial progenitor cells (EPCs). However, the contribution functional role EPCs in tumor neoangiogenesis are controversial. Therefore, using genetically marked BM cells, we demonstrate precise spatial temporal to neovascularization three transplanted one spontaneous breast vivo high-resolution microscopy flow cytometry. We show that early tumors recruit BM-derived differentiate...

10.1101/gad.436307 article EN Genes & Development 2007-06-15

Abstract The vascular endothelial growth factor (VEGF) plays a key role in tumor angiogenesis. However, clinical trials targeting the VEGF pathway are often ineffective, suggesting that other factors/pathways also important We have previously shown Notch ligand Delta-like 4 (DLL4) is up-regulated vasculature. Here, we show DLL4, when expressed cells, functions as negative regulator of angiogenesis by reducing number blood vessels all five types xenografts, but acts positive driver for two...

10.1158/0008-5472.can-07-0969 article EN Cancer Research 2007-12-01

Translocations involving the NUP98 gene produce NUP98-fusion proteins and are associated with a poor prognosis in acute myeloid leukemia (AML). MLL1 is molecular dependency leukemia, therefore we investigated efficacy of therapeutic blockade menin-MLL1 interaction models. Using mouse cell lines driven by NUP98-HOXA9 NUP98-JARID1A fusion oncoproteins, demonstrate that NUP98-fusion-driven sensitive to inhibitor VTP50469, an IC50 similar what have previously reported for MLL-rearranged NPM1c...

10.1182/blood.2021012806 article EN cc-by Blood 2021-09-28

Receptor editing is believed to play the major role in purging newly formed B cell compartments of autoreactivity by induction secondary V(D)J rearrangements. In process immunoglobulin heavy (H) chain editing, these rearrangements are mediated direct VH-to-JH joining or cryptic recombination signals (cRSs) within VH gene segments. Using a statistical model RS, we have identified potential cRSs segments at conserved sites flanking complementarity-determining regions 1 and 2. These active...

10.1084/jem.20071224 article EN The Journal of Experimental Medicine 2007-12-03

Jonathan D. Powell, Emily B. Heikamp, Kristen N. Pollizzi and Adam T. Waickman Department of Oncology, Johns Hopkins University School Medicine, Baltimore, Maryland 21231 Correspondence: poweljo{at}jhmi.edu

10.1101/sqb.2013.78.020214 article EN Cold Spring Harbor Symposia on Quantitative Biology 2013-01-01

Abstract Higher order chromatin structure and DNA methylation are implicated in multiple developmental processes, but their relationship to cell state is unknown. Here, we found that large (~10kb) nadirs can form long loops connecting anchor loci may be dozens of megabases apart, as well interchromosomal links. The interacting comprise ~3.5Mb the human genome. data more consistent with formation these by phase separation a genomic subcompartment, rather than CTCF-mediated extrusion....

10.1101/212928 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2017-11-09

NUP98 fusion oncoproteins (FOs) are a hallmark of childhood acute myeloid leukemia (AML) and drive leukemogenesis through liquid-liquid phase separation-mediated nuclear condensate formation. However, the composition consequences FO-associated condensates incompletely understood. Here we show that MYST family histone acetyltransferase (HAT) complex proteins including MOZ/KAT6A, HBO1/KAT7, common MOZ/HBO1 subunit BRPF1 associate with FOs on chromatin within condensates. HATs molecular...

10.1101/2024.12.02.624182 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-12-05

Epigenetic therapies are emerging for pediatric cancers. Due to the relatively low mutational burden in tumors, epigenetic dysregulation and differentiation blockade is a hallmark of oncogenesis some childhood By targeting regulators that maintain tumor cells primitive developmental state, may induce differentiation. The most well-studied clinically advanced epigenetic-targeted include azacitidine decitabine, which inhibit DNA methylation through competitive inhibition enzymatic activity...

10.1101/cshperspect.a041637 article EN Cold Spring Harbor Perspectives in Medicine 2024-12-18

10.1016/j.jpeds.2017.09.041 article EN The Journal of Pediatrics 2017-11-22

Abstract The mechanistic target of rapamycin is an essential regulator T cell metabolism and differentiation. In this study, we demonstrate that serum- glucocorticoid-regulated kinase 1 (SGK1), a downstream node complex 2 signaling, represses memory CD8+ During acute infections, murine SGK1-deficient cells adopt early precursor phenotype leading to more long-lived cells. Thus, enhanced recall capacity in response reinfection can readily reject tumors. Mechanistically, activation results...

10.4049/jimmunol.2100669 article EN The Journal of Immunology 2022-12-15

10.1016/j.jpeds.2016.08.023 article EN The Journal of Pediatrics 2016-12-20
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