About

Chi Van Dang, MD, PhD, is an Adjunct Professor of Medicine (Hematology-Oncology) at the Perelman School of Medicine at the University of Pennsylvania. He is affiliated with the Abramson Cancer Center and specializes in internal medicine. His educational background includes a BS in Chemistry from the University of Michigan (1975), a PhD in Chemistry from Georgetown University (1978), and an MD from Johns Hopkins University School of Medicine (1982).

Research topics

• Genetics
• Biology
• Computational biology
• Cancer research
• Medicine
• Bioinformatics
• Immunology

Selected publications

• Green synthesis and recognition of Cr₂O₇2− and CrO₄2− ions of a novel Schiff base fluorescent probe

  Inorganica Chimica Acta · 2026-02-07

  article
  PublisherDOI

• FigureS1 from Androgen Receptor Drives Polyamine Synthesis, Creating a Vulnerability for Prostate Cancer

  2026-03-02

  articleOpen access

  <p>SPA increases intracellular and extracellular polyamines in prostate cancer cell lines</p>

  PublisherDOI

• Clock Regulation of Metabolites Reveals Coupling between Transcription and Metabolism

  UNC Libraries · 2026-01-14

  articleOpen access
  PublisherDOI

• FigureS7 from Androgen Receptor Drives Polyamine Synthesis, Creating a Vulnerability for Prostate Cancer

  2026-03-02

  articleOpen access

  <p>dCas9-KRAB blocks AR binding upstream of ODC1</p>

  PublisherDOI

• FigureS4 from Androgen Receptor Drives Polyamine Synthesis, Creating a Vulnerability for Prostate Cancer

  2026-03-02

  articleOpen access

  <p>AR-V7 can positively regulate ODC</p>

  PublisherDOI

• FigureS5 from Androgen Receptor Drives Polyamine Synthesis, Creating a Vulnerability for Prostate Cancer

  2026-03-02

  articleOpen access

  <p>SPA does not alter abundance of hypusinated eIF5A</p>

  PublisherDOI

• Androgen Receptor Drives Polyamine Synthesis, Creating a Vulnerability for Prostate Cancer

  Cancer Research · 2025-11-21 · 1 citations

  articleOpen access

  Supraphysiologic androgen (SPA) treatment can paradoxically restrict the growth of castration-resistant prostate cancer (CRPC) with high androgen receptor (AR) activity, which is the basis for the use of bipolar androgen therapy (BAT) for patients with this disease. Although androgens are widely appreciated for enhancing anabolic metabolism, how SPA-mediated metabolic changes alter prostate cancer progression and therapy response is unknown. In this study, we report that SPA markedly increased intracellular and secreted polyamines in prostate cancer models. AR binding at enhancer sites upstream of the ornithine decarboxylase 1 (ODC1) promoter increased the abundance of ODC, a rate-limiting enzyme of polyamine synthesis, and de novo synthesis of polyamines from arginine. SPA-stimulated polyamines enhanced prostate cancer fitness, as dCas9-KRAB-mediated inhibition of AR regulation of ODC1 or direct ODC inhibition by difluoromethylornithine (DFMO) increased the efficacy of SPA. Mechanistically, AR activation combined with the loss of negative feedback by polyamines increased the activity of S-adenosylmethionine decarboxylase 1, leading to the depletion of its substrate, S-adenosylmethionine, and global protein methylation. These data provided the rationale for a clinical trial testing the safety and efficacy of BAT in combination with DFMO for patients with metastatic CRPC. Pharmacodynamic studies of this therapeutic combination in the first five patients in the trial indicated that this approach effectively depleted polyamines in plasma. Thus, the AR potently stimulates polyamine synthesis, which constitutes a vulnerability in prostate cancer treated with SPA that can be targeted therapeutically. SIGNIFICANCE: Increased polyamine synthesis is a prominent metabolic change induced by the androgen receptor that drives tumor progression and confers a targetable vulnerability in advanced prostate cancer. See related commentary by Alizadeh-Ghodsi and Goldstein, p. 1095.

  PublisherOA PDFDOI

• Green synthesis of Schiff base based on thiadiazolyl and recognition of arginine and ascorbic acid

  Spectrochimica Acta Part A Molecular and Biomolecular Spectroscopy · 2025-06-12

  article
  PublisherDOI

• Lineage dependence of the neuroblastoma surfaceome defines tumor cell state-dependent and -independent immunotherapeutic targets

  Neuro-Oncology · 2025-01-17 · 6 citations

  articleOpen access

  BACKGROUND: Neuroblastoma is a heterogeneous disease with adrenergic (ADRN)-like cells and therapy-resistant mesenchymal (MES)-like cells driven by distinct transcription factor networks. Here, we investigate the expression of immunotherapeutic targets in each neuroblastoma subtype and propose pan-neuroblastoma and cell state-specific targetable cell surface proteins. METHODS: We characterized cell lines, patient-derived xenografts, and patient samples as ADRN-dominant or MES-dominant to define subtype-specific and pan-neuroblastoma gene sets. Targets were validated with ChIP-sequencing, immunoblotting, and flow cytometry in neuroblastoma cell lines and isogenic ADRN-to-MES transition cell line models. Finally, we evaluated the activity of MES-specific agents in vivo and in vitro. RESULTS: Most immunotherapeutic targets being developed for neuroblastoma showed significantly higher expression in the ADRN subtype with limited expression in MES-like tumor cells. In contrast, CD276 (B7-H3) and L1CAM maintained expression across both ADRN and MES states. We identified several receptor tyrosine kinases (RTKs) enriched in MES-dominant samples and showed that AXL targeting with ADCT-601 was potently cytotoxic in MES-dominant cell lines and showed specific antitumor activity in a MES cell line-derived xenograft. CONCLUSIONS: Immunotherapeutic strategies for neuroblastoma must address the potential of epigenetic downregulation of antigen density as a mechanism for immune evasion. We identified several RTKs as candidate MES-specific immunotherapeutic target proteins for the elimination of therapy-resistant cells. We hypothesize that the phenomena of immune escape will be less likely when targeting pan-neuroblastoma cell surface proteins such as B7-H3 and L1CAM, and/or dual targeting strategies that consider both the ADRN and MES cell states.

  PublisherOA PDFDOI

• Imaging the uptake and metabolism of glutamine in prostate tumor models using CEST MRI

  npj Imaging · 2025-08-01 · 3 citations

  articleOpen access

  Glutamine metabolism is upregulated in many cancers. While multiple glutamine imaging agents have been developed and translated to clinical use, the short half-lives of their signal and instability in vivo limit the aspects of glutamine metabolism they capture. In phantoms at physiological pH, chemical exchange saturation transfer (CEST) magnetic resonance imaging (MRI) contrast was observed at 11.7 T from glutamine, downstream metabolic products (glutamate and ammonia) and their co-substrates (alanine, aspartate, and cystine/cysteine). This contrast increased at lower pH. These results suggest that both uptake and metabolism of glutamine would increase CEST signal enhancement. We then investigated the feasibility of imaging the uptake (delivery, transport and metabolism) of naturally-occuring glutamine using CEST MRI in preclinical prostate cancer models, wherein key metabolic proteins are the glutamine transporter ASCT2 and as well as enzymes GLS1, ALT2 (GPT2), AST1 (GOT1), and GDH1 (GLUD1). The LNCaP prostate cancer line exhibited higher expression of ASCT2, GDH1, ALT2, and AST1 compared to DU-145 cells. CEST MRI enhancement upon administration of glutamine was consistently higher in LNCaP 3D spheres (phantoms) and tumors (in vivo) than their DU-145 counterparts. Mass spectrometry imaging confirmed higher uptake and metabolism of glutamine in LNCaP tumors. These findings demonstrate that CEST MRI of glutamine is capable of distinguishing preclinical prostate tumor models that differ in glutamine uptake and has potential for translation to clinical use.

  PublisherOA PDFDOI

Recent grants

• Defining the Role of the Cancer Circadian Clock in Tumor Immunity and Tumorigenesis

  NIH · $371k · 1990–2025

• Defining the Role of the Cancer Circadian Clock in Tumor Immunity and Tumorigenesis

  NIH · $5.7M · 1990–2026

• Training Program in Hematology

  NIH · $8.1M · 1982–2030

• NIH Grant G13LM007515

  NIH · $198k · 2004

• NIH Grant R37CA051497

  NIH · $3.2M · 2007

Frequent coauthors

• Brian J. Altman

  University of Rochester

  138 shared

• Karen Zeller

  133 shared

• Zachary E. Stine

  The Wistar Institute

  112 shared

• Anne Le

  109 shared

• Annie L. Hsieh

  Massachusetts General Hospital

  99 shared

• Rebekah Brooks

  The Wistar Institute

  69 shared

• Takashi Tsukamoto

  Johns Hopkins Medicine

  62 shared

• Angelo M. De Marzo

  60 shared

Labs

• Chi Van Dang LaboratoryPI

Education

• Hematology-Oncology Fellow, Cancer Research Institute

  University of California San Francisco

  1987

• Internship, Osler Medical Resident, Medicine

  Johns Hopkins Hospital

  1985

• MD, School of Medicine

  Johns Hopkins Medicine

  1982

• PhD, Chemistry, Chemistry

  Georgetown University

  1978

• BS, Chemistry

  University of Michigan

  1975