The Destination for Pharmacy Education

Harrison College of Pharmacy

Faculty and Staff Directory

David Riese

David Riese

Franklin Professor
Unit: Drug Discovery and Development
Auburn University
Harrison College of Pharmacy
3211g Walker Building
Auburn, AL 36849
Phone: 334-844-8358
Fax: 334-844-8353



  • A.B., Summa Cum Laude, Biology - Wabash College, 1987
  • M.Phil., Human Genetics - Yale University, 1989
  • Ph.D., Genetics - Yale University, 1993

Professional History

1993-95: Postdoctoral Fellow, Department of Pathology - Yale University

1995-97: Associate Research Scientist, Department of Pathology, Yale University

1997-2010: Assistant/Associate Professor, Department of Medicinal Chemistry and Molecular Pharmacology, Purdue University

1997-2010: Assistant/Associate Professor, Purdue University Center for Cancer Research

2010-18: Adjunct Professor, Department of Medicinal Chemistry and Molecular Pharmacology, Purdue University

2010-18: Associate Dean for Research and Graduate Programs, Auburn University Harrison College of Pharmacy

2010-21: Gilliland Endowed Professor, Department of Drug Discovery and Development, Auburn University Harrison College of Pharmacy

2020-present: Senior Scientist, Cancer Biology and Immunology Program, O’Neal Comprehensive Cancer Center, University of Alabama-Birmingham

2021-present: Professor, Department of Drug Discovery and Development, Auburn University Harrison College of Pharmacy

Current Funding

Targeted Melanoma Therapy: Identification of ERBB4 Melanoma Driver Mutants
Auburn University Intramural Grants Program
Role: Principal Investigator
Total Cost: $50,000

Laboratory Personnel

Graduate Students

  • Vipasha Dwivedi
  • Lauren Lucas
  • Rania Mohamedelhassan

External Links

Research Interests

Overview – We study the Epidermal Growth Factor (EGF) family of peptide hormones and their receptors, the ErbB receptor tyrosine kinases. This network regulates the proliferation and differentiation of epithelial cells and deregulated signaling by this network contributes to human tumorigenesis and increased tumor cell invasiveness, metastatic potential, and chemoresistance. Consequently, we seek to understand the mechanism by which this network regulates cell function, with the ultimate goal being the development of novel cancer treatments.

ERBB4 Signaling and ERBB4 Inhibitors – We have demonstrated that ERBB4 homodimers function as tumor suppressor proteins, whereas ERBB4-EGFR and ERBB4-ERBB2 heterodimers function as oncogenes. We are focused on deciphering the mechanisms by which ERBB4 can be coupled to these divergent responses [19, 25, 26, 41, 44, 50, 57]. We are also pursuing the discovery and development of novel ERBB4 agonists and antagonists that can be used to pharmacologically probe ERBB4 function in human malignancies and hold potential for the treatment of ErbB4-dependent tumors [30, 36, 42, 46, 55].

ERBB4 in Human Tumors – We have reviewed the roles that ERBB4 and its ligands play in human tumors [51, 57]. These reviews summarize the rationale for several projects underway in our laboratory. Metastatic melanomas that possess wild type (WT) BRAF alleles are particularly deadly, as they do not respond to BRAF inhibitors, MEK inhibitors, or other targeted chemotherapeutics. Our preliminary data indicate that ERBB4 heterodimers function as oncogenes in human melanoma cell lines that possess BRAF WT alleles. We are developing in silico methods to assess whether ERBB4 mutations found in BRAF WT melanoma samples function are likely to function as melanoma drivers [56]. We are utilizing in vitro and in vivo model systems to define the roles of ERBB4 overexpression, ERBB4 heterodimerization partners, ERBB4 ligands, and ERBB4 mutations in BRAF WT human melanoma. Similar but less advanced efforts are underway to determine the role of ERBB4 signaling in human childhood brain tumors and triple negative cancers.

Selected Publications

#Contributes to my Google Scholar i10-Index of 49

*Contributes to my Google Scholar H-index of 35 

  • #*19. EE Williams, LJ Trout, RM Gallo, SE Pitfield, DJ Penington, I Bryant, and DJ Riese II.  A constitutively-active ErbB4 mutant inhibits drug-resistant colony formation by the DU-145 and PC-3 human prostate tumor cell lines. Cancer Lett 192: 67-74 (2003).  PMID: 12637154
  • #25. RM Gallo, I Bryant, R Fry, EE Williams, and DJ Riese II. Phosphorylation of ErbB4 on Tyr1056 is critical for inhibition of colony formation by prostate tumor cell lines. Biochem Biophys Res Com 349: 372-382 (2006).  PMID: 16934755
  • #26. SE Pitfield, I Bryant, DJ Penington, G Park, and DJ Riese II. Phosphorylation of ErbB4 on tyrosine 1056 is critical for ErbB4 coupling to inhibition of colony formation by human mammary cell lines.  Oncol Res 16: 179-193 (2006).   PMID: 17120616
  • #30. KJ Wilson, CP Mill, EM Cameron, SS Hobbs, RP Hammer, and DJ Riese II. Interconversion of Neuregulin2 full and partial agonists for ErbB4. Biochem Biophys Res Com 364: 351-357 (2007). PMID: 17945187
  • #*36. KJ Wilson, JL Gilmore, J Foley, MA Lemmon, and DJ Riese II.  Functional selectivity of EGF Family Peptide Growth Factors: Implications for Cancer. Pharmacol Ther 122: 1-8 (2009). PMID: 19135477
  • #41. CP Mill, K Gettinger, and DJ Riese II. Ligand stimulation of ErbB4 and a constitutively-active ErbB4 mutant result in different biological responses in human pancreatic tumor cell lines. Exp Cell Res 317: 392-404 (2011).  PMID: 21110957
  • #42. DJ Riese II. Ligand-based receptor tyrosine kinase partial agonists: New paradigm for cancer drug discovery?  Expert Opin Drug Disc 6: 185-193 (2011). PMID: 21532939
  • #*44. CP Mill, MD Zordan, SM Rothenberg, J Settleman, JF Leary, and DJ Riese II. ErbB2 is necessary for ErbB4 ligands to stimulate oncogenic activities in models of human breast cancer. Genes & Cancer 2: 792-804 (2011). PMID: 22393464
  • 46. KJ Wilson, CP Mill, RM Gallo, EM Cameron, H VanBrocklin, J Settleman, and DJ Riese II. The Q43L mutant of Neuregulin 2beta is a pan-ErbB receptor antagonist. Biochem J 443: 133-144 (2012). PMID: 22216880
  • #50. RM Gallo, IN Bryant, CP Mill, S Kaverman, and DJ Riese II.  Multiple functional motifs are required for the tumor suppressor activity of a constitutively-active ErbB4 mutant.  J Cancer Res Ther Oncol 1: 104 (2013). PMID: 24791013
  • #*51. DJ Riese II and RL Cullum. Epiregulin: Roles in Normal Physiology and Cancer. Sem Cell Dev Biol28: 49-56 (2014). PMID 24631357
  • 55. RL Cullum, LM Lucas, JI Senfeld, JT Piazza, LT Neel, K Whig, L Zhai, MH Harris, CC Rael, DC Taylor, LJ Cook, DP Kaufmann, CP Mill, MA Jacobi, FT Smith, M Suto, R Bostwick, RB Gupta, AE David, and DJ Riese II. Development and application of high-throughput screens for the discovery of compounds that disrupt ErbB4 signaling: Candidate cancer therapeutics.  PLOS One 15: (12) e0243901 (2020).  PMID: 33378376
  • 56. RL Cullum and DJ Riese II. The simulated random assignment of missense mutations throughout a gene of interest can determine whether missense mutations found in that gene in a population of tumor genomes are non-randomly distributed. (2021). DOI
  • 57.  LM Lucas, V Dwivedi, J Senfeld, RL Cullum, CP Mill, JT Piazza, IN Bryant, LJ Cook, ST Miller, C Kelley, E Knerr, J Markham, D Kaufmann, M Jacobi, J Shen, and DJ Riese II.  The yin and yang of ERBB4: Tumor suppressor and oncogene.  Pharm Rev 74: 18-47 (2022).  PMID: 34987087

Last Updated: August 04, 2022