Elliot O. Eton

ORCID: 0000-0002-8980-9310
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About
Contact & Profiles
Research Areas
  • RNA Interference and Gene Delivery
  • Immunotherapy and Immune Responses
  • Nanoparticle-Based Drug Delivery
  • Cancer Genomics and Diagnostics
  • Heat shock proteins research
  • Multiple Myeloma Research and Treatments
  • Monoclonal and Polyclonal Antibodies Research
  • Immunodeficiency and Autoimmune Disorders
  • Otitis Media and Relapsing Polychondritis
  • Immune Cell Function and Interaction
  • Autoimmune and Inflammatory Disorders Research
  • MicroRNA in disease regulation
  • Cancer Immunotherapy and Biomarkers
  • CRISPR and Genetic Engineering
  • Metabolism, Diabetes, and Cancer
  • Cancer-related Molecular Pathways
  • Advanced biosensing and bioanalysis techniques
  • RNA regulation and disease
  • RNA modifications and cancer
  • Immune cells in cancer
  • Cancer, Hypoxia, and Metabolism
  • Chronic Lymphocytic Leukemia Research
  • Bacteriophages and microbial interactions
  • Lung Cancer Treatments and Mutations
  • Chronic Myeloid Leukemia Treatments

Weill Cornell Medicine
2023-2024

New York Genome Center
2023-2024

Cornell University
2023-2024

Memorial Sloan Kettering Cancer Center
2024

Rockefeller University
2024

Tri-Institutional PhD Program in Chemical Biology
2024

Brigham and Women's Hospital
2019-2023

Broad Institute
2020

Harvard University
2018-2019

Abstract Somatic evolution leads to the emergence of clonal diversity across tissues with broad implications for human health. A striking example somatic is VEXAS (Vacuoles E1 enzyme X-linked Autoinflammatory Somatic) syndrome, caused by UBA1 mutations in hematopoietic stem cells (HSCs), inducing treatment-refractory, systemic inflammation. However, mechanisms that lead survival and expansion mutant HSCs are unknown, limiting development effective therapies. The lack animal or cellular...

10.1101/2024.05.19.594376 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-05-20

Understanding intrinsic and acquired resistance is crucial to overcoming cancer chemotherapy failure. While it well-established that intratumor, subclonal genetic phenotypic heterogeneity significantly contribute resistance, not fully understood how tumor sub-clones interact with each other withstand therapy pressure. Here, we report a previously unrecognized behavior in heterogeneous tumors: cooperative adaptation (CAT), which cells induce co-resistant phenotypes neighboring when exposed...

10.1371/journal.pcbi.1007278 article EN cc-by PLoS Computational Biology 2019-08-26

Abstract Drug-induced resistance, or tolerance, is an emerging yet poorly understood failure of anticancer therapy. The interplay between drug-tolerant cancer cells and innate immunity within the tumor, consequence on tumor growth, therapeutic strategies to address these challenges remain undescribed. Here, we elucidate role taxane-induced resistance natural killer (NK) cell in triple-negative breast (TNBC) design spatiotemporally controlled nanomedicines, which boost efficacy invigorate...

10.1158/0008-5472.can-19-4036 article EN Cancer Research 2020-10-19

Engineered macromolecules offer compelling means for the therapy of conventionally undruggable interactions in human disease. However, their efficacy is limited by barriers to tissue and intracellular delivery. Inspired recent advances molecular barcoding evolution, we developed BarcodeBabel, a generalized method design libraries peptide barcodes suitable high-throughput mass spectrometry proteomics. Combined with PeptideBabel, Monte Carlo sampling algorithm peptides evolvable...

10.1021/acs.jproteome.4c00068 article EN Journal of Proteome Research 2024-05-22

<div>Abstract<p>Drug-induced resistance, or tolerance, is an emerging yet poorly understood failure of anticancer therapy. The interplay between drug-tolerant cancer cells and innate immunity within the tumor, consequence on tumor growth, therapeutic strategies to address these challenges remain undescribed. Here, we elucidate role taxane-induced resistance natural killer (NK) cell in triple-negative breast (TNBC) design spatiotemporally controlled nanomedicines, which boost...

10.1158/0008-5472.c.6512503.v1 preprint EN 2023-03-31

<div>Abstract<p>Drug-induced resistance, or tolerance, is an emerging yet poorly understood failure of anticancer therapy. The interplay between drug-tolerant cancer cells and innate immunity within the tumor, consequence on tumor growth, therapeutic strategies to address these challenges remain undescribed. Here, we elucidate role taxane-induced resistance natural killer (NK) cell in triple-negative breast (TNBC) design spatiotemporally controlled nanomedicines, which boost...

10.1158/0008-5472.c.6512503 preprint EN 2023-03-31

Abstract Background: Triple negative breast cancer (TNBC) is an aggressive basal-like malignancy, which recurs more frequently than any other subtype of cancer. We recently discovered that TNBC can overcome drug pressure by switching to a hybrid (CD44Hi) and epithelial-like (CD24Hi) cell state, accompanied transient period quiescence, or dormancy. These dormant, ‘hybrid' cells highly express the phosphorylated SRC family kinase, hematopoietic kinase (HCK). Methods: Here, we used panel novel...

10.1158/1538-7445.am2018-51 article EN cc-by-nc Cancer Research 2018-07-01

Understanding intrinsic and adaptive resistance is crucial to overcoming multiple myeloma chemotherapy failure. We recently demonstrated that standard can induce cancer cells phenotypically transition a transient state of dormancy drug tolerance. Further, targeting precisely during this thwart the emergence (Goldman, 2015). However, it not yet understood how stromal contexture may contribute chemotherapy-induced tolerance.We developed deterministic mathematical model containing system...

10.1158/1538-7445.sabcs18-694 article EN Bioinformatics, Convergence Science, and Systems Biology 2019-07-01

Abstract Understanding intrinsic and adaptive resistance is crucial to overcoming multiple myeloma chemotherapy failure. We recently demonstrated that standard can induce cancer cells phenotypically transition a transient state of dormancy drug tolerance. Further, targeting precisely during this thwart the emergence (Goldman, 2015). However, it not yet understood how stromal contexture may contribute chemotherapy-induced developed deterministic mathematical model containing system...

10.1158/1538-7445.am2019-694 article EN Cancer Research 2019-07-01
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