Deborah J. Veis , MD, PhD

Deborah J. Veis , MD, PhD

Professor of Medicine and Pathology and Immunology

Dr. Veis (Novack) received her undergraduate degree in Molecular Biology from Princeton University, Princeton, NJ; completed the MD/PhD program at Washington University; and was a postdoctoral fellow in the laboratory of Steven Teitelbaum. She is board certified in Anatomic Pathology with expertise in bone and breast diseases; and joined our Division in 2003.  She has served in the leadership of the American Society for Bone and Mineral Research and the American Society for Clinical Investigation.  She currently serves as the Director of the Histology and Histomorphometry Core, Musculoskeletal Research Center.  Dr. Veis’s research focuses on the role of NF-κB in osteoclastogenesis and bone resorption, and the role of this pathway in pathological osteolysis and in the host response to metastasis.  She also studies the role of mitochondria in bone cell biology.  Dr. Veis also has extensive collaborations with clinicians on studies related to bone disease and breast cancer.

Editorial Responsibilities

  • Editorial Board: Journal of Bone and Mineral Research
  • Reviewer: Cell, Developmental Cell, Cancer Cell, Journal of Clinical Investigation, Journal of Biological Chemistry, Journal of Bone and Mineral Research, Arthritis and Rheumatism, Blood, Cell Death and Differentiation, American Journal of Pathology, Calcified Tissue International

Professional Societies and Organizations

  • American Medical Association
  • American Society for Bone and Mineral Research
  • American Society of Clinical Pathology
  • College of American Pathologists
  • American Society for Clinical Investigation


  • ASBMR Career Enhancement Award, American Society for Bone and Mineral Research, 2007
  • Harold Frost Young Investigator Award, American Society for Bone and Mineral Research, 2004
  • ASBMR Young Investigator Award, American Society for Bone and Mineral Research, 2001
  • Spencer T. and Ann Olin Award for Excellence in Graduate Research, Washington University, 1993
  • Phi Beta Kappa, Princeton University, 1987
  • DBBS Graduate Program Affiliation
  • Molecular Cell Biology

Clinical Interests

  • Anatomic and Molecular Pathology – Metabolic Bone Pathology
  • Anatomic and Molecular Pathology – Breast Pathology

Research Interests

My lab has focused on the study of osteoclasts, the cells that resorb/remove bone to allow normal bone turnover. These cells are hematopoietic-derived cells of the monocyte lineage that differentiate in the bone microenvironment under the influence of the cytokine RANKL. Osteoclasts attach to the bone surface via integrins and form an extracellular compartment, the resorption lacuna, into which they secrete acid and proteases to degrade the organic and mineral components of bone. Activity of these cells is critical for bone homeostasis, but their abnormal activation is responsible for pathological bone loss in many settings, including osteolytic breast cancer metastases. Our work has centered on the role of NF-kB signaling in osteoclasts, particularly in the context of cancer metastasis to bone and inflammatory arthritis. NF-kB activation is known to be involved in the inflammatory response in autoimmune diseases, and it also plays important but complex roles in the pathogenesis of many types of cancer, including breast cancer. Because NF-kB is active in so many cell types, with different physiological effects, it is important to understand the role of NF-kB in bone cells, as well as in specific tumor and immune cells. We employ a variety of knockout and transgenic mice, as well as pharmacological treatments that either inhibit or activate specific NF-kB pathways, using a combination of bioluminescent imaging, microCT, and histomorphometric analyses. Our ultimate goal is to guide the development of therapies that preserve bone structure and function while effectively targeting tumor and immune cells. My clinical research interests include analyzing bone biopsies for studies of metabolic bone diseases such as osteoporosis and hypophosphatasia, using both qualitative and quantitative histomorphometric approaches. In addition, I work with clinicians to describe new or rare bone diseases. In the future I hope to combine my laboratory studies of breast cancer bone metastasis with analysis of clinical samples to better translate our findings to patients.


  • Vaira, S., Johnson, T., Hirbe, A.C., Alhawagri, M., Anwisye, I., Sammut, B., O’Neal, J., Zou, W., Weilbaecher, K.N., Faccio, R., and Novack, D.V.. RelB is the NF-kB subunit downstream of NIK responsible for osteoclast differentiation. Proc Natl Acad Sci 105:3897-3902, 2008
  • Vaira, S., Alhawagri, M., Anwisye, I., Kitaura, H., Faccio, R., and Novack, D.V. RANKL activates an apoptotic JNK pathway opposed by RelA/p65. J Clin Invest 118:2088-2097, 2008.
  • Armamento-Villareal R, Napoli N, Diemer K, Watkins M, Civitelli R, Teitelbaum S, Novack D. Bone turnover in bone biopsies of patients with low-energy cortical fractures receiving bisphosphonates: a case series. Calcif Tissue Int 85:37-44, 2009
  • Whyte MP, Wenkert D, McAlister WH, Novack D, Nenninger AR, Zhang X, Huskey M, Mumm S.. Dysosteosclerosis presents as an “osteoclast-poor” form of osteopetrosis: Comprehensive investigation of a 3-year-old girl and literature review. J Bone Miner Res [Epub ahead of print]
  • Yang C, McCoy K, Davis JL, Schmidt-Supprian M, Sasaki Y, Faccio R, Novack DV. NIK Stabilization in Osteoclasts Results in Osteoporosis and Enhanced Inflammatory Osteolysis. PLoS One, in press, 2010