Erin M. Taylor
Researcher
Also affiliated: Brigham and Women's Hospital (2019–2025); National Institutes of Health (2010); Beth Israel Deaconess Medical Center (2017–2021); Mount Sinai Hospital (2015); NewYork–Presbyterian Hospital (2013–2018); Harvard University (2017–2025); University of California, Los Angeles (2010); University of Dundee (2010); Cornell University (2014); Universidade do Estado do Pará (2019); University of Exeter (2025); University of Michigan (2015); Royal Derby Hospital (1990); Columbia University Irving Medical Center (2013–2018); Leicester Royal Infirmary (1988); American Society of Plastic Surgeons (2015); New York Hospital Queens (2013–2014); Action for ME (2021); Freeman Hospital (2024); Johns Hopkins University Applied Physics Laboratory (2011); Massachusetts General Hospital (2020); University of Texas Health Science Center at Dallas (2016); Mount Sinai Medical Center (2015); Presbyterian Hospital (2014); Musculoskeletal Transplant Foundation (2019); Mount Sinai Hospital (2015); National Institute of Neurological Disorders and Stroke (2010); Michigan United (2015); North Middlesex Hospital (1992); Rush University (2017); Columbia University (2015); Icahn School of Medicine at Mount Sinai (2015)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Erin M. Taylor investigates various aspects of health and disease, with recent work focusing on cancer research and the management of lymphedema. Taylor has published research on the role of TCF1–LEF1 co-expression in allergic diseases and the potential of CRISPR/dCas9-KRAB-mediated suppression of S100b to restore p53-mediated apoptosis in melanoma cells. Additionally, Taylor is involved in studies examining the treatment outcomes for chronic breast cancer-associated lymphedema, including the protocol for the international multicenter trial comparing microsurgical and conservative treatments. Other research areas include the surgical management of hidradenitis suppurativa and protocols for pneumothorax treatment. Taylor's scholarship metrics include an h-index of 14 with 57 total publications and 736 citations. Key collaborators at the University of Arkansas for Medical Sciences include Brian Koss, Aaron J. Storey, Samrat Roy Choudhury, and Sara C. Shalin.
Metrics
- h-index: 14
- Publications: 57
- Citations: 776
Selected Publications
-
Abstract 4622: Proteomic insights into anti-CTLA4 therapy resistance in metastatic melanoma: Pathway-specific biomarkers for treatment response (2025)
-
CRISPR/dCas9-KRAB-Mediated Suppression of S100b Restores p53-Mediated Apoptosis in Melanoma Cells (2023)
-
Proteomic signatures of innate immunity in immunotherapy naïve melanomas correlate with anti-CTLA-4 immunotherapy responsiveness (2020)
-
Epigenetic Control of <i>Cdkn2a.Arf</i> Protects Tumor-Infiltrating Lymphocytes from Metabolic Exhaustion (2020)
-
Proteogenomic analysis of melanoma brain metastases from distinct anatomical sites identifies pathways of metastatic progression (2020)
-
Abstract 1029: Epigenetic control of tumor-infiltrating lymphocyte metabolic-exhaustion (2020)
-
Histone Modifications as Biomarkers for Immunotherapy (2019)
-
Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma (2019)
-
Quantitative microinjection using fluorescence calibration of streaming microdroplets on a superhydrophobic surface (2018)
-
Abstract LB-206: Indicators of responsiveness to immune checkpoint inhibitors (2017)
-
Indicators of responsiveness to immune checkpoint inhibitors (2017)
Collaboration Network
Top Collaborators
- CRISPR/dCas9-KRAB-Mediated Suppression of S100b Restores p53-Mediated Apoptosis in Melanoma Cells
- Abstract 4622: Proteomic insights into anti-CTLA4 therapy resistance in metastatic melanoma: Pathway-specific biomarkers for treatment response
- CRISPR/dCas9-KRAB-Mediated Suppression of S100b Restores p53-Mediated Apoptosis in Melanoma Cells
- Abstract 4622: Proteomic insights into anti-CTLA4 therapy resistance in metastatic melanoma: Pathway-specific biomarkers for treatment response
- CRISPR/dCas9-KRAB-Mediated Suppression of S100b Restores p53-Mediated Apoptosis in Melanoma Cells
- CRISPR/dCas9-KRAB-Mediated Suppression of S100b Restores p53-Mediated Apoptosis in Melanoma Cells
- CRISPR/dCas9-KRAB-Mediated Suppression of S100b Restores p53-Mediated Apoptosis in Melanoma Cells
- Abstract 4622: Proteomic insights into anti-CTLA4 therapy resistance in metastatic melanoma: Pathway-specific biomarkers for treatment response
Similar Researchers
Based on overlapping research topics