Thomas M. Ruenger, MD, PhD

Portrait Ruenger

Professor and Vice-Chair for Clinical and Academic Affairs

Director, International Graduate Training Program in Dermatology

Boston University School of Medicine

Physician Director of Outpatient Clinical Services

 

Administrative

Boston University Medical Center

609 Albany Street, Boston, MA 02118

Office: 617.638.5500 Fax: 617.638.5515

 

Education

1985 MD Medical School of Christian-Albrecht University, Kiel, Germany
1986-1989 Postdoctoral Fellowship Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD (with Dr. Kenneth H. Kraemer)
1989-1992 Residency Department of Dermatology, Julius-Maximilian University, Wurzburg, Germany. German Board Certification in Dermatology 1992
1994 Residency Allergology, Department of Dermatology, Julius-Maximilian University, Wurzburg, Germany. German Board Certification in Allergology 1994
1994 PhD (equiv) “Habilitation”, Medical School of Julius-Maximilian University, Wurzburg, Germany

Clinical Specialties and Research Interests

Clinical: Phototherapy, photodermatology, psoriasis, cutaneous lymphona, general medical dermatology

Research: Photobiology and photodermatology, DNA repair, skin cancer, extracellular matrix (wound healing, scleroderma)

 

Summary

Thomas M. Ruenger, MD PhD joined the Department of Dermatology at Boston University in 1999. Before that, he was Professor and Vice-Chairman of the Department of Dermatology at  the Georg August University in Göttingen, Germany, and now is Professor and Vice-Chairman for Clinical and Academic Affairs of the Department of Dermatology at Boston University. While practicing general medical dermatology, including pediatric dermatology, his main clinical interests are in photodermatology, in particular phototherapy and skin diseases with photosensitivity, and skin oncology, in particular cutaneous lymphomas. As a physician scientist, he provides not only clinical care to patients, but also pursues his research interest in his laboratory. His clinical interests in photodermatology are mirrored in his research interests in photobiology of skin cells, including UV-induced DNA damage, DNA repair, and other cellular DNA damage responses. A particular interest of his is how longwave ultraviolet light (UVA) causes mutations and with that skin cancer. In recent years, his research interests have expanded to the field of extracellular matrix biology. In particular, he has described a novel mechanism by which skin cells degrade the extracellular matrix proteins collagen and elastin, which may be of high clinical relevance for wound healing, scleroderma, and tumor invasion. Dr. Ruenger is the recipient of several academic, scientific, and teaching awards and he serves on the editorial board of four prestigious journals in dermatology and photobiology and on the Board of Directors of the Photomedicine Society. He is also the director of the International Graduate Training Program in Dermatology at Boston University. He is fluent in his native German and in Spanish.

Selected Publications

  1. Rünger TM, Adami S, Benhamou CL, Czerwinski E, Farrerons J, Kendler DL, Mindeholm L, Realdi G, Roux C, Smith V (2010) Morphea-like skin reactions in patients treated with the cathepsin K inhibitor Balicatib. Journal of the American Academy of Dermatology in press
  2. Rizzo J, Dunn J, Rees A, Rünger TM (2010) No formation of DNA double strand breaks and no activation of recombination repair with UVA, Journal of Investigative Dermatology advanced online publication doi:10.1038/jid.2010.365
  3. Rünger TM (2008) Invited Commentary: C à T transition mutations are not solely UVB-signature mutations, because they are also generated by UVA. Journal of Investigative Dermatology 128, 2138 – 2140
  4. Rünger TM, Quintanilla-Dieck MJ, Bhawan J (2007) Role of cathepsin K in the turnover of the dermal extracellular matrix during scar formation. Journal of Investigative Dermatology 127, 293 – 297
  5. Dunn J, Potter M, Rees A, Rünger TM (2006) Activation of the Fanconi anemia/BRCA pathway and recombination repair in the cellular response to solar ultraviolet light. Cancer Research 66, 11140 – 11147
  6. Kappes UP, Luo D, Potter M,  Schulmeister K, Rünger TM (2006) Short- and long-wave ultraviolet light (UVB and UVA) induce similar mutations in human skin cells. Journal of Investigative Dermatology 126, 667 – 675
  7. Sarkar P, Vergilis I, Sharpless NE, DePinho R, Rünger TM (2004) Loss of p16INK4a or p19ARF confers deficient repair of DNA photoproducts. Journal of the National Cancer Institute 96, 1790 – 1793