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Associate Vice President for UI Health AllianceEA Crowell, Jr Professor and Chair of SurgeryProfessor of Surgery
- Surgical Oncology and Endocrine SurgeryProfessor of
Anatomy and Cell Biology
Primary Office: 1509 JCPIowa City, IA 52242
Primary Office Phone: 319-353-7474
MS, Chemical Engineering, Massachusetts Institute of TechnologyMD, Yale University School of MedicinePhD, Molecular Biophysics and Biochemistry, Yale University Graduate SchoolMBA, The Wharton School, University of Pennsylvania
Research Assistant, Department of Chemical Engineering, Massachusetts Institute of Technology Cambridge, MAGraduate Student, Department of Chemical Engineering, Massachusetts Institute of Technology Cambridge, MAInternship, Duke University Medical CenterPost Doctoral, Fellowship, Department Microbiology/ Immunology, Duke University Medical Center Durham, NCResidency, Duke University Medical Center
Iowa Medical License, Iowa Board of MedicineCertified, Advanced Trauma Life SupportBoard Certified, American Board of Surgery
Biosciences Graduate ProgramDepartment of Biochemistry PhDMedical Scientist Training Program
The Weigel laboratory has had a long-standing interest in determining mechanisms of hormone response in breast cancer. Our work has identified transcriptional mechanisms that regulate the expression of estrogen receptor- alpha in breast carcinomas. Other areas of investigation have sought to identify genes that are related to hormone response and additional mechanisms of gene regulation that are responsive to estrogen. Current Projects Regulation of ER by AP2 . We identified the AP2? transcription factor as a key regulator of hormone response in breast cancer. We are now examining mechanisms of gene regulation that involve this transcription factor. Chromatin Effects Altering AP2 Activity. We have shown that epigenetic chromatin alterations can influence activity of AP2 at certain promoters. The mechanism appears to involve altered binding of AP2 mediated through chromatin structure. Studies to determine how chromatin structure alters AP2 activity are being pursued. Interaction of AP2 and p53. We demonstrated a direct interaction between AP2 factors and the p53 tumor suppressor. The interaction of p53 and AP2 has functional effects on these two factors that appear to alter hormone response in breast cancer and cell growth in other cancer types. We are investigating the details of this interaction and the functional effects on gene regulation and cell physiology.
Expression of the RET Proto-oncogene is Regulated by TFAP2C in Breast Cancer Independent of the Estrogen Receptor.
Annals of Surgical Oncology .
2012. Guidroz J,
Sampling of secondary margins decreases the need for re-excision after partial mastectomy.
2011 October. 150(4):802-9.
Surveillance and intervention after thyroid lobectomy.
Ann Surg Oncol.
2011 June. 18(6):1729-33.
Discovery of SMAD4 Promoters, Transcription Factor Binding Sites, and Deletions in Juvenile Polyposis Patients.
Nucleic Acids Research.
PET-CT scans in recurrent or persistent differentiated thyroid cancer: is there added utility beyond conventional imaging?.
2010 December. 148(6):1082-9; discussion 1089-90.
Discovery of the BMPR1A promoter and germline mutations that cause juvenile polyposis.
Hum Mol Genet.
2010 December 1. 19(23):4654-62.
Identification of primary gene targets of TFAP2C in hormone responsive breast carcinoma cells.
Genes Chromosomes Cancer.
2010 October. 49(10):948-62.
Risk factors for development and recurrence of primary breast abscesses.
J Am Coll Surg.
2010 July. 211(1):41-8.
Date Last Modified: 02/28/2014 -
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