David T. Woodley, MD

Professor of Dermatology

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Overview

Dr. Woodley was trained in Dermatology in Chapel Hill at the University of North Carolina. He was a Research Fellow at the University of Paris/Rothschild Institute for two years and an Expert Investigator at the National Institutes of Health. He later joined the dermatology faculty at the University of North Carolina where he started the Phototherapy Unit for the treatment of psoriasis.

In 1988, he became professor and vice chair of the Department of Dermatology at Stanford University and ran the Stanford Psoriasis Center and the Immunodermatology Lab. In 1992, he was appointed the Walter J. Hamlin Professor and Chair of the Department of Dermatology at Northwestern University.

In 1999, he joined USC as professor and co-chief of the Division of Dermatology. In 2005, dermatology became an independent academic department, and Dr. Woodley was appointed professor and chair of the new department. He has published over 165 scientific papers and has had continuous NIH funding since 1982.

Research Funding

  • A Pilot Study of the Effect of Intravenous Gentamicin on the Restoration of Full-Length Type VII Collagen in RDEB Patients Carrying Nonsense Mutations
    NIH · R21AR071716 · Mar 1, 2018 – Feb 28, 2021 · Role: Co-Principal Investigator
  • The Role of Exogenous Type VII Collagen on the Healing of Skin Wounds
    NIH · I01BX002028 · Jul 1, 2014 – Jun 30, 2023 · Role: Principal Investigator
  • Protein Therapy for Recessive Dystrophic Epidermolysis Bullosa
    NIH · RC4AR060535 · Sep 20, 2010 – Sep 30, 2013 · Role: Co-Principal Investigator
  • Mechanism of Keratinocyte Motility
    NIH · R01AR046538 · Mar 24, 1999 – Apr 30, 2011 · Role: Principal Investigator
  • POST GRADUATE PROGRAM IN CUTANEOUS BIOLOGY
    NIH · T32AR007593 · Jul 1, 1995 – Jun 30, 2006 · Role: Co-Principal Investigator
  • CHARACTERIZATION OF EDIDERMOLYSIS BULLOSA ANTIGEN
    NIH · K04AR001540 · Sep 30, 1985 – Nov 30, 1990 · Role: Principal Investigator
  • Purification of Epidermolysis Bullosa Antigen
    NIH · R01AR033625 · Apr 1, 1984 – Aug 31, 2015 · Role: Principal Investigator
  • PURIFICATION OF EPIDERMOLYSIS BULLOSA ACQUISITA ANTIGEN
    NIH · R01AM033625 · Apr 1, 1984 – Mar 31, 1987 · Role: Principal Investigator

Publications

  • Targeting Hsp90 in Cancer for 25 Years: Failure of Previous Clinical Trials and New Hope for Future Therapeutics. Cells. 2025 12 15; 14(24).. View in PubMed
  • Therapeutic Opportunities in Overcoming Premature Termination Codons in Epidermolysis Bullosa via Translational Readthrough. Cells. 2025 Aug 07; 14(15).. View in PubMed
  • Previously unrecognized and potentially consequential challenges facing Hsp90 inhibitors in cancer clinical trials. Cell Stress Chaperones. 2024 10; 29(5):642-653.. View in PubMed
  • Pseudopemphigoid: A systematic review. JAAD Int. 2024 Dec; 17:170-171.. View in PubMed
  • Splice modulation strategy applied to deep intronic variants in COL7A1 causing recessive dystrophic epidermolysis bullosa. Proc Natl Acad Sci U S A. 2024 08 27; 121(35):e2401781121.. View in PubMed
  • Discovery of Cell Number-Interstitial Fluid Volume (CIF) Ratio Reveals Secretory Autophagy Pathway to Supply eHsp90α for Wound Healing. Cells. 2024 07 30; 13(15).. View in PubMed
  • Intravenous gentamicin therapy induces functional type VII collagen in patients with recessive dystrophic epidermolysis bullosa: an open-label clinical trial. Br J Dermatol. 2024 07 16; 191(2):267-274.. View in PubMed
  • Correction: Evolutionarily conserved dual lysine motif determines the non-chaperone function of secreted Hsp90alpha in tumour progression. Oncogene. 2024 May; 43(18):1397-1398.. View in PubMed
  • Highly Efficient Ex Vivo Correction of COL7A1 through Ribonucleoprotein-Based CRISPR/Cas9 and Homology-Directed Repair to Treat Recessive Dystrophic Epidermolysis Bullosa. J Invest Dermatol. 2024 Jun; 144(6):1322-1333.e13.. View in PubMed
  • Expression of Concern: Participation of the lipoprotein receptor LRP1 in hypoxia-HSP90α autocrine signaling to promote keratinocyte migration. J Cell Sci. 2023 11 01; 136(21).. View in PubMed