About

Julia I-Ju Leu, PhD, is a Research Associate Professor of Genetics at the University of Pennsylvania's Perelman School of Medicine. She is part of the Department of Genetics and is based at the Clinical Research Building in Philadelphia. Her educational background includes a B.S. in Cell and Molecular Biology from the University of Washington in 1994 and a Ph.D. in Cell and Molecular Biology from the University of Pennsylvania in 2001. Her research focuses on the functional interplay among redox signaling, metabolism, and ferroptosis, particularly in relation to genetic variants of the tumor suppressor gene TP53. Dr. Leu's work involves understanding how these molecular pathways influence cancer development and response to therapy, with a specific interest in redox regulation and tumor suppression mechanisms.

Research topics

• Biology
• Cancer research
• Chemistry
• Cell biology
• Molecular biology

Selected publications

• Table S4 from An African-Specific Variant of <i>TP5</i>3 Reveals PADI4 as a Regulator of p53-Mediated Tumor Suppression

  2025-12-11

  articleOpen access

  <p>Extra crystallographic data for p53Y107H.</p>

  PublisherDOI

• Supplementary Figures S1-S8 from An African-Specific Variant of <i>TP5</i>3 Reveals PADI4 as a Regulator of p53-Mediated Tumor Suppression

  2025-12-11

  articleOpen access

  <p>Supplementary Figure S1. The Y107H variant of p53 is comparable to WT p53 for growth suppression and apoptosis. Supplementary Figure S2. The Y107H variant is impaired for transactivation of a subset of p53 target genes, including PADI4, PLTP, and HHAT. Supplementary Figure S3. The Y107H protein is impaired for binding to p53 response elements. Supplementary Figure S4. Structural analysis of the Y107H variant shows similar structure but decreased thermal stability and increased propensity to misfold into mutant p53 conformation. Supplementary Figure S5. Mice with the Y107H variant have increased cancer risk. Supplementary Figure S6. Colorectal cancer cells harboring hypomorphic variants have increased sensitivity to the glutaminase inhibitor CB-839. Supplementary Figure S7. PADI4 is a p53 target and has tumor suppressive activity. Supplementary Figure S8. PADI4 correlates with increased immune signatures and wild-type p53 in human cancers.</p>

  PublisherDOI

• Table S1 from An African-Specific Variant of <i>TP5</i>3 Reveals PADI4 as a Regulator of p53-Mediated Tumor Suppression

  2025-12-11

  articleOpen access

  <p>RNA-seq of top genes identified in Y107H vs WT LCLs, related to Figure 2.</p>

  PublisherDOI

• Table S2 from An African-Specific Variant of <i>TP5</i>3 Reveals PADI4 as a Regulator of p53-Mediated Tumor Suppression

  2025-12-11

  articleOpen access

  <p>Evaluating the association between AA, Y107H variant, and cancer risk.</p>

  PublisherDOI

• Table S5 from An African-Specific Variant of <i>TP5</i>3 Reveals PADI4 as a Regulator of p53-Mediated Tumor Suppression

  2025-12-11

  articleOpen access

  <p>Secondary Validations of top drug hits from HCT116 WT vs Y107H clones.</p>

  PublisherDOI

• Mutant p53 binds and controls estrogen receptor activity to drive endocrine resistance in ovarian cancer

  Genes & Development · 2025-11-05 · 2 citations

  articleOpen access

  High-grade serous ovarian cancer (HGSOC) is a highly lethal gynecologic malignancy in women. Women diagnosed with HGSOC initially respond to chemotherapy, but there is a >80% rate of relapse. There is thus a significant unmet need for new therapeutic targets for HGSOC. Estrogen receptor α (ERα) is a particularly attractive candidate, as ∼70% of HGSOC tumors stain positively for ERα and there are approved inhibitors that show limited toxicity. However, unlike the case for breast cancer, endocrine therapy for HGSOC has not shown consistently promising results. In this work, we show that missense mutant forms of p53, which occur in >60% of HGSOC, bind and inhibit ERα function and confer resistance to fulvestrant and elacestrant. Mechanistically, we show that mutant p53 predominantly inhibits one arm of the ERα pathway—the transactivation of jointly regulated ERα–SP1 target genes such as the mTOR regulator DEPTOR . We show that silencing mutant p53 restores the ability of ERα to transactivate ERα–SP1 target genes and renders HGSOC markedly more sensitive to endocrine therapy. Consistent with this premise, we show that the p53 mutant Y220C refolding compound rezatapopt enhances fulvestrant response in a Y220C mutant cell line.

  PublisherOA PDFDOI

• Table S6 from An African-Specific Variant of <i>TP5</i>3 Reveals PADI4 as a Regulator of p53-Mediated Tumor Suppression

  2025-12-11

  articleOpen access

  <p>Key Reagents List for this study.</p>

  PublisherDOI

• Table S3 from An African-Specific Variant of <i>TP5</i>3 Reveals PADI4 as a Regulator of p53-Mediated Tumor Suppression

  2025-12-11

  articleOpen access

  <p>Oligos for ChIP-qPCR and qPCR used in this study</p>

  PublisherDOI

• Table S1 from An African-specific variant of TP53 reveals PADI4 as a regulator of p53-mediated tumor suppression

  2024-09-16

  preprintOpen access

  <p>RNA-seq of top genes identified in Y107H vs WT LCLs, related to Figure 2.</p>

  PublisherDOI

• Table S6 from An African-specific variant of TP53 reveals PADI4 as a regulator of p53-mediated tumor suppression

  2024-09-16

  preprintOpen access

  <p>Key Reagents List for this study.</p>

  PublisherDOI

Recent grants

• NIH Grant F32CA112715

  NIH · $102k · 2007

• Modulators of liver injury

  NIH · $595k · 2007–2012

Frequent coauthors

• Maureen E. Murphy

  The Wistar Institute

  140 shared

• Donna L. George

  90 shared

• Qin Liu

  Nanjing Drum Tower Hospital

  88 shared

• Andrew V. Kossenkov

  84 shared

• Thibaut Barnoud

  MUSC Hollings Cancer Center

  67 shared

• Alexandra Indeglia

  65 shared

• Jessica C. Leung

  61 shared

• Joel Cassel

  The Wistar Institute

  59 shared

Labs

• Leu LaboratoryPI