Douglas E. Feldman, PhD

Research Assistant Professor of Pathology (Part-Time)

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Overview

Dr. Feldman’s research team studies the following major topic areas:

1. Immunomodulation and immune engineering for the treatment of inflammation and fibrosis.
2. Roles of modified DNA bases in immune signaling and gene control.
2. Functional analysis of viral counter-immune systems.

Categories: Gene Control, Stem Cells, Cancer, Epigenetics, DNA modification, immune engineering, immunotherapy, fibrosis, AALD

Education and Training

  • Harvard College, Cambridge, MA. — A.B. Magna cum laude — Biochemistry
  • Stanford University, Stanford, CA. — Ph.D — Molecular Cell Biology

Research Funding

  • Activation of NK cell-mediated protective immunity for the systemic treatment of ALD
    NIH · R21AA029741 · Sep 11, 2023 – Aug 31, 2025 · Role: Principal Investigator
  • Activation of NK cell-mediated protective immunity for the systemic treatment of ALD
    NIH · 1R21AA029741-01A1 · Sep 1, 2023 – Aug 31, 2025 · Role: PI
  • STING-Activating CAR-NK Cell Therapy
    US DOD CDMRP · Aug 15, 2022 – Feb 14, 2024 · Role: PI
  • Engineering CAR-T for treatment of alcoholic liver disease
    NIH · R21AA027535 · Sep 20, 2019 – Aug 31, 2021 · Role: PI
  • Robert E. and May R. Wright Foundation Trust
    Robert E. and May R. Wright Foundation Trust
  • American Cancer Society
    American Cancer Society
  • James H. Zumberge Faculty Research and Innovation Fund
    James H. Zumberge Faculty Research and Innovation Fund

Publications

  • Hypoxia and the unfolded protein response. Methods Enzymol. 2007; 435:275-93.. View in PubMed
  • Identification of mitogen-activated protein kinase signaling pathways that confer resistance to endoplasmic reticulum stress in Saccharomyces cerevisiae. Mol Cancer Res. 2005 Dec; 3(12):669-77.. View in PubMed
  • The unfolded protein response: a novel component of the hypoxic stress response in tumors. Mol Cancer Res. 2005 Nov; 3(11):597-605.. View in PubMed
  • Tumorigenic mutations in VHL disrupt folding in vivo by interfering with chaperonin binding. Mol Cell. 2003 Nov; 12(5):1213-24.. View in PubMed