Iowa City, IA 52242
MS, Chemical Engineering, Massachusetts Institute of Technology
MD, Yale University School of Medicine
PhD, Molecular Biophysics and Biochemistry, Yale University Graduate School
MBA, The Wharton School, University of Pennsylvania
Internship, Duke University Medical Center
Post Doctorate, Fellowship, Department Microbiology/ Immunology, Duke University Medical Center
Chief Resident, Duke University Medical Center
Licensure and Certifications
Iowa Medical License, Iowa Board of Medicine
Pennsylvania Medical License
California Medical License
North Carolina Medical License
Certified, Advanced Trauma Life Support
Board Certified, American Board of Surgery
Education/Training Program Affiliations
Department of Biochemistry PhD
Medical 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.
Park J, Wu T, Cyr A, Woodfield G, De Andrade J, Spanheimer P, Li T, Sugg S, Lal G, Domann F, Zhang W, Weigel R. The role of Tcfap2c in tumorigenesis and cancer growth in an activated Neu model of mammary carcinogenesis.. Oncogene. 2015 March 16.
Cyr A, Kulak M, Park J, Bogachek M, Spanheimer P, Woodfield G, White-Baer L, O'Malley Y, Sugg S, Olivier A, Zhang W, Domann F, Weigel R. TFAP2C governs the luminal epithelial phenotype in mammary development and carcinogenesis.. Oncogene. 2015 January 22. 34(4):436-44.
Bogachek M, De Andrade J, Weigel R. Regulation of epithelial-mesenchymal transition through SUMOylation of transcription factors.. Cancer research. 2015 January 1. 75(1):11-5.
Bogachek M, Chen Y, Kulak M, Woodfield G, Cyr A, Spanheimer P, Li Y, Li T, Weigel R. Sumoylation Pathway Is Required to Maintain the Basal Breast Cancer Subtype. Cancer Cell. 2014 June. 25:748-761.
Spanheimer P, Cyr A, Gillum M, Woodfield G, Askeland R, Weigel R. Distinct Pathways Regulated by RET and ER in Luminal Breast Cancer Demonstrates the Biologic Basis for Combination Therapy. Annals of Surgery. 2014 April. 259:793-799.
Spanheimer P, Park J, Askeland R, Kulak M, Cyr A, Woodfield G, Sugg S, Thomas A, Weigel R, . Inhibition of RET Increases the Efficacy of Antiestrogen and Is a Novel Treatment Strategy for Luminal Breast Cancer.. Clinical Cancer Research. 2014 April. 20:2115-2125.
Lal G, Gomez-Contreras P, Kulak M, Woodfield G, Bair T, Domann F, Weigel R. Human melanoma cells over-express Extracellular Matrix 1 (ECM1) which is regulated by TFAP2C. PLOS ONE; 2013.
Kulak M, Cyr A, Woodfield G, Bogachek M, Li T, Price D, Domann F, Weigel R. Transcriptional Regulation of the GPX1 Gene by TFAP2C and Aberrant CpG Methylation in Human Breast Cancer. Oncogene . 2012 September. 32:4043-4051.
Spanheimer P, Woodfield G, Cyr A, Kulak M, White-Baer L, Bair T, Weigel R. Expression of the RET Proto-oncogene is Regulated by TFAP2C in Breast Cancer Independent of the Estrogen Receptor. Annals of Surgical Oncology . 2012 August. 20:2204-2212.
Woodfield G, Chen Y, Bair T, Domann F, Weigel R. Identification of primary gene targets of TFAP2C in hormone responsive breast carcinoma cells. Genes Chromosomes Cancer. 2010 October. 49(10):948-62.