About

John DiGiovanni, Ph.D., is a Professor of Pharmacology & Toxicology and the Coulter R. Sublett Chair at the University of Texas at Austin College of Pharmacy. His research focuses on understanding how cancer develops, with an emphasis on identifying novel targets, mechanisms, and strategies for cancer prevention. His work explores gene-environment interactions involved in cancer, aiming to understand early cellular, biochemical, and molecular changes that transform normal cells into cancer cells. His laboratory investigates cellular signaling pathways disrupted during tumor development, including the PI3K/Akt/mTOR pathway and Stats proteins, particularly Stats1, 3, and 5. A significant aspect of his research involves identifying target cells, such as keratinocyte stem cells, which are major targets for skin tumor initiation, and studying genes that confer susceptibility to environmentally-induced cancers, including mapping susceptibility loci in mice and examining their relevance to human cancers. Recently, his research has expanded to study the impact of obesity on cancer development and progression, including early-life obesity, with a focus on molecular targets and signaling pathways affected by obesity in tissues related to skin, prostate, head and neck, and lymphoma cancers. His work aims to uncover mechanisms underlying increased cancer risk associated with obesity and to develop strategies to mitigate this risk.

Research topics

• Biochemistry
• Biology
• Cancer research
• Chemistry
• Genetics
• Cell biology
• Pharmacology

Selected publications

• A Combination of Xanthohumol and Ursolic Acid in the Diet Leads to Synergistic Inhibition of Prostate Cancer Progression

  Molecular Carcinogenesis · 2026-02-10

  articleOpen accessSenior authorCorresponding

  Prostate cancer (PCa) is the second most common cancer and second leading cause of cancer death for American men. Chemoprevention by using phytochemicals offers a promising approach to improve outcomes due to their ability to act on cancer cell metabolism and growth while maintaining low toxicity profiles. The goal of this study was to assess the combination of xanthohumol (XAN) and ursolic acid (UA) given in the diet for synergistic efficacy against PCa progression and identify potential mechanisms of action. PCa cells were treated with the combination to evaluate cell survival and colony formation. Two mouse models of PCa were used to evaluate tolerability and efficacy of dietary administration of the combination and to further understand mechanism(s) of action. The combination of XAN + UA reduced PCa cell survival and colony formation. The combination given in the diet significantly and synergistically inhibited growth of HMVP2 PCa allograft tumors and also inhibited PCa progression in HiMyc mice. Mechanistically, inhibition of polyamine synthesis and epithelial-to-mesenchymal transition contributed to the inhibition of HMVP2 allograft tumor growth, while the inhibition of PCa progression in HiMyc mice was associated with activation of the unfolded protein response pathway and apoptosis. Further studies in cultured PCa cells revealed additional effects of the combination on several oncogenic signaling pathways (e.g, phospho-STAT3) and cell cycle regulatory proteins (e.g, cyclin D1, phospho-Rb).

  PublisherDOI

• Supplementary Figure 2 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage

  2025-06-03

  preprintOpen access

  <p>Using pentanucleotide signature to define novel DMBA signature</p>

  PublisherOA PDFDOI

• Supplementary Figure 8 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage

  2025-06-03

  preprintOpen access

  <p>Recurrently observed driver mutations and co-mutation frequencies</p>

  PublisherOA PDFDOI

• Supplementary Figure 7 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage

  2025-06-03

  preprintOpen access

  <p>Driver mutations observed in chemically induced tumors or spontaneously derived tumors</p>

  PublisherOA PDFDOI

• Supplementary Dataset from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage

  2025-06-03

  preprintOpen access

  <p>List of top differentially expressed genes in the high versus low BMI tumor study</p>

  PublisherDOI

• Supplementary Table 1 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage

  2025-06-03

  supplementary-materialsOpen access

  <p>Summary of SNV mutations observed by tumor model and subgroup</p>

  PublisherOA PDFDOI

• GLP-1 Agonist Use Among Men With Localized Prostate Cancer: A Narrative Review and Rationale for Prospective Clinical Trials

  Urology · 2025-05-09 · 2 citations

  reviewOpen access
  PublisherOA PDFDOI

• Supplementary Figure 4 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage

  2025-06-03

  preprintOpen access

  <p>Inflammation-driven mutations may be associated with timing of exposure during development</p>

  PublisherOA PDFDOI

• Supplementary Figure 6 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage

  2025-06-03

  preprintOpen access

  <p>Inflammation is the time limiting step in tumorigenesis in LGR5/6-Cre activated KRAS/HRAS mouse</p>

  PublisherOA PDFDOI

• GLP-1 Agonist Use Among Men with Localized Prostate Cancer: A Narrative Review and Rationale for Prospective Clinical Trials

  SSRN Electronic Journal · 2025-01-01

  reviewOpen access
  PublisherDOI

Recent grants

• NIH Grant R01CA189623

  NIH · $2.9M · 2020

• NIH Grant R01ES016623

  NIH · $1.7M · 2014

• NIH Grant R01CA037111

  NIH · $4.9M · 2012

• Targeting Androgen Receptor and PARP for Synthetic Lethality in CRPC

  NIH · $46.7M · 2009–2023

• NIH Grant R01CA099526

  NIH · $1.7M · 2008

Frequent coauthors

• Achinto Saha

  The University of Texas at Austin

  110 shared

• Linda Beltrán

  101 shared

• Kaoru Kiguchi

  98 shared

• Jorge Blando

  AstraZeneca (United States)

  98 shared

• Okkyung Rho

  84 shared

• Thomas J. Slaga

  78 shared

• Steve Carbajal

  73 shared

• Ronald G. Harvey

  69 shared

Education

• Ph.D., Phrmacology

  The University of Washington