Clinical Focus

  • Dermatology
  • Wound healing
  • Fibrosis

Academic Appointments

Professional Education

  • Board Certification: American Board of Dermatology, Dermatology (2023)
  • Residency: Stanford University Dermatology Residency (2023) CA
  • Internship: Medstar Harbor Hospital Internal Medicine Residency (2020) MD
  • MD, Harvard Medical School, Medicine (2019)
  • PhD, Massachusetts Institute of Technology, Biology (2017)
  • Bachelor of Arts, Harvard College, Molecular and Cellular Biology (2011)

Stanford Advisors

Current Research and Scholarly Interests

Wound healing, cutaneous fibrosis

All Publications

  • Adult-onset inflammatory linear verrucous epidermal nevus successfully treated with intralesional steroid. JAAD case reports Johnson, A. N., Sum, K., Rieger, K. E., Chiou, A. S., Li, D. J. 2024; 46: 5-7

    View details for DOI 10.1016/j.jdcr.2024.02.001

    View details for PubMedID 38445192

  • Pioglitazone Decreases Adipogenisis Leading to Melanoma Skin Tumor Suppression Downer, M., Griffin, M., Morgan, A., Parker, J. B., Berry, C., Li, D. J., Liang, N., Kameni, L., Wan, D. C., Longaker, M. T. LIPPINCOTT WILLIAMS & WILKINS. 2023: S387-S388
  • A Review of Radiation-Induced Vascular Injury and Clinical Impact. Annals of plastic surgery Kameni, L. E., Januszyk, M., Berry, C. E., Downer, M. A., Parker, J. B., Morgan, A. G., Valencia, C., Griffin, M., Li, D. J., Liang, N. E., Momeni, A., Longaker, M. T., Wan, D. C. 2023


    ABSTRACT: The number of cancer survivors continues to increase because of advances in therapeutic modalities. Along with surgery and chemotherapy, radiotherapy is a commonly used treatment modality in roughly half of all cancer patients. It is particularly helpful in the oncologic treatment of patients with breast, head and neck, and prostate malignancies. Unfortunately, among patients receiving radiation therapy, long-term sequalae are often unavoidable, and there is accumulating clinical evidence suggesting significant radiation-related damage to the vascular endothelium. Ionizing radiation has been known to cause obliterative fibrosis and increased wall thickness in irradiated blood vessels. Clinically, these vascular changes induced by ionizing radiation can pose unique surgical challenges when operating in radiated fields. Here, we review the relevant literature on radiation-induced vascular damage focusing on mechanisms and signaling pathways involved and highlight microsurgical anastomotic outcomes after radiotherapy. In addition, we briefly comment on potential therapeutic strategies, which may have the ability to mitigate radiation injury to the vascular endothelium.

    View details for DOI 10.1097/SAP.0000000000003723

    View details for PubMedID 37962260

  • Understanding the Role of Adipocytes and Fibroblasts in Cancer. Annals of plastic surgery Downer, M. A., Griffin, M. F., Morgan, A. G., Parker, J. B., Li, D. J., Berry, C. E., Liang, N. E., Kameni, L., Cotterell, A. C., Akras, D., Valencia, C., Longaker, M. T., Wan, D. C. 2023


    Cancer is currently the second leading cause of death in the United States. There is increasing evidence that the tumor microenvironment (TME) is pivotal for tumorigenesis and metastasis. Recently, adipocytes and cancer-associated fibroblasts (CAFs) in the TME have been shown to play a major role in tumorigenesis of different cancers, specifically melanoma. Animal studies have shown that CAFs and adipocytes within the TME help tumors evade the immune system, for example, by releasing chemokines to blunt the effectiveness of the host defense. Although studies have identified that adipocytes and CAFs play a role in tumorigenesis, adipocyte transition to fibroblast within the TME is fairly unknown. This review intends to elucidate the potential that adipocytes may have to transition to fibroblasts and, as part of the TME, a critical role that CAFs may play in affecting the growth and invasion of tumor cells. Future studies that illuminate the function of adipocytes and CAFs in the TME may pave way for new antitumor therapies.

    View details for DOI 10.1097/SAP.0000000000003658

    View details for PubMedID 37553786

  • Assessment of Need for Improved Identification of a Culprit Drug in Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis. JAMA dermatology Li, D. J., Velasquez, G. A., Romar, G. A., Schunkert, E. M., Foreman, R. K., Divito, S. J. 2023


    Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) is a severe hypersensitivity reaction. Identifying a culprit drug is critical for patient care, yet identification is based on clinical judgment. Data are limited on the accuracy in or approach to identifying a culprit drug.To evaluate patient allergy list outcomes, current approaches in identifying culprit drugs, and potential methods of improving culprit drug identification.This retrospective cohort study spanned 18 years (January 2000 to July 2018), was conducted at Brigham and Women's Hospital and Massachusetts General Hospital (Boston), and included patients with clinically and histologically confirmed cases of SJS/TEN overlap and TEN.This study descriptively analyzed potential culprits to SJS/TEN, patients' allergy lists, and currently used approaches that led to those lists. It then tested the theoretical contribution of incorporating various parameters to allergy list outcomes.Of 48 patients (29 women [60.4%]; 4 Asian [8.3%], 6 Black [12.5%], 5 Hispanic [10.4%], and 25 White [52.1%] individuals; median age, 40 years [range, 1-82 years]), the mean (SD) number of drugs taken per patient at disease onset was 6.5 (4.7). Physicians labeled 17 patients as allergic to a single culprit drug. Comparatively, 104 drugs were added to allergy lists across all patients. Physicians' approaches relied largely on heuristic identification of high-notoriety drugs and the timing of drug exposure. Use of a vetted database for drug risk improved sensitivity. Algorithm for Drug Causality for Epidermal Necrolysis scoring was discordant in 28 cases, labeling an additional 9 drugs missed by physicians and clearing 43 drugs labeled as allergens by physicians. Human leukocyte antigen testing could have potentially affected 20 cases. Consideration of infection as a culprit was limited.The results of this cohort study suggest that currently used approaches to identify culprit drugs in SJS/TEN are associated with overlabeling patients allergic to likely nonculprit drugs and less commonly missed possible culprit drugs. Incorporation of a systematized unbiased approach could potentially improve culprit drug identification, although ultimately a diagnostic test is necessary.

    View details for DOI 10.1001/jamadermatol.2023.1693

    View details for PubMedID 37342052

  • Histologic features of graft-versus-host disease-associated angiomatosis: Insights into pathophysiology and treatment JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY Li, D. J., Romar, G. A., Hsieh, P., Wells, M., Foreman, R. K., Lian, C. G., Divito, S. J. 2020; 83 (3): 914-917

    View details for DOI 10.1016/j.jaad.2019.12.058

    View details for Web of Science ID 000562322300058

    View details for PubMedID 31923444

    View details for PubMedCentralID PMC7931771

  • Muscle and neuronal guidepost-like cells facilitate planarian visual system regeneration SCIENCE Scimone, M., Atabay, K. D., Fincher, C. T., Bonneau, A. R., Li, D. J., Reddien, P. W. 2020; 368 (6498): 1447-+


    Neuronal circuits damaged or lost after injury can be regenerated in some adult organisms, but the mechanisms enabling this process are largely unknown. We used the planarian Schmidtea mediterranea to study visual system regeneration after injury. We identify a rare population of muscle cells tightly associated with photoreceptor axons at stereotyped positions in both uninjured and regenerating animals. Together with a neuronal population, these cells promote de novo assembly of the visual system in diverse injury and eye transplantation contexts. These muscle guidepost-like cells are specified independently of eyes, and their position is defined by an extrinsic array of positional information cues. These findings provide a mechanism, involving adult formation of guidepost-like cells typically observed in embryos, for axon pattern restoration in regeneration.

    View details for DOI 10.1126/science.aba3203

    View details for Web of Science ID 000545264600033

    View details for PubMedID 32586989

    View details for PubMedCentralID PMC8128157

  • A Patient With Widespread Painful Purpura JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION Li, D. J., Laga, A. C., Imadojemu, S. 2019; 322 (19): 1914-1915

    View details for DOI 10.1001/jama.2019.15276

    View details for Web of Science ID 000501356100023

    View details for PubMedID 31609398

  • Nuclear receptor NR4A is required for patterning at the ends of the planarian anterior-posterior axis ELIFE Li, D. J., McMann, C. L., Reddien, P. W. 2019; 8


    Positional information is fundamental to animal regeneration and tissue turnover. In planarians, muscle cells express signaling molecules to promote positional identity. At the ends of the anterior-posterior (AP) axis, positional identity is determined by anterior and posterior poles, which are putative organizers. We identified a gene, nr4A, that is required for anterior- and posterior-pole localization to axis extremes. nr4A encodes a nuclear receptor expressed predominantly in planarian muscle, including strongly at AP-axis ends and the poles. nr4A RNAi causes patterning gene expression domains to retract from head and tail tips, and ectopic anterior and posterior anatomy (e.g., eyes) to iteratively appear more internally. Our study reveals a novel patterning phenotype, in which pattern-organizing cells (poles) shift from their normal locations (axis extremes), triggering abnormal tissue pattern that fails to reach equilibrium. We propose that nr4A promotes pattern at planarian AP axis ends through restriction of patterning gene expression domains.

    View details for DOI 10.7554/eLife.42015

    View details for Web of Science ID 000468967100001

    View details for PubMedID 31025936

    View details for PubMedCentralID PMC6534381

  • Landmarks in Existing Tissue at Wounds Are Utilized to Generate Pattern in Regenerating Tissue CURRENT BIOLOGY Oderberg, I. M., Li, D. J., Scimone, M., Gavino, M. A., Reddien, P. W. 2017; 27 (5): 733-742


    Regeneration in many organisms involves the formation of a blastema, which differentiates and organizes into the appropriate missing tissues. How blastema pattern is generated and integrated with pre-existing tissues is a central question in the field of regeneration. Planarians are free-living flatworms capable of rapidly regenerating from small body fragments [1]. A cell cluster at the anterior tip of planarian head blastemas (the anterior pole) is required for anterior-posterior (AP) and medial-lateral (ML) blastema patterning [2-4]. Transplantation of the head tip into tails induced host tissues to grow patterned head-like outgrowths containing a midline. Given the important patterning role of the anterior pole, understanding how it becomes localized during regeneration would help explain how wounds establish pattern in new tissue. Anterior pole progenitors were specified at the pre-existing midline of regenerating fragments, even when this location deviated from the ML median plane of the wound face. Anterior pole progenitors were specified broadly on the dorsal-ventral (DV) axis and subsequently formed a cluster at the DV boundary of the animal. We propose that three landmarks of pre-existing tissue at wounds set the location of anterior pole formation: a polarized AP axis, the pre-existing midline, and the dorsal-ventral median plane. Subsequently, blastema pattern is organized around the anterior pole. This process, utilizing positional information in existing tissue at unpredictably shaped wounds, can influence the patterning of new tissue in a manner that facilitates integration with pre-existing tissue in regeneration.

    View details for DOI 10.1016/j.cub.2017.01.024

    View details for Web of Science ID 000396297100027

    View details for PubMedID 28216315

    View details for PubMedCentralID PMC5801735