Thomas M Rünger

Summary

Affiliation: Boston University
Country: USA

Publications

  1. doi request reprint Much remains to be learned about how UVR induces mutations
    Thomas M Rünger
    Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts 02118, USA USA
    J Invest Dermatol 133:1717-9. 2013
  2. doi request reprint Morphea-like skin reactions in patients treated with the cathepsin K inhibitor balicatib
    Thomas M Rünger
    Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    J Am Acad Dermatol 66:e89-96. 2012
  3. doi request reprint Comparison of DNA damage responses following equimutagenic doses of UVA and UVB: a less effective cell cycle arrest with UVA may render UVA-induced pyrimidine dimers more mutagenic than UVB-induced ones
    Thomas M Rünger
    Boston University School of Medicine, Department of Dermatology, 609 Albany Street, Boston, MA 02118, USA
    Photochem Photobiol Sci 11:207-15. 2012
  4. ncbi request reprint C-->T transition mutations are not solely UVB-signature mutations, because they are also generated by UVA
    Thomas M Rünger
    Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts, USA
    J Invest Dermatol 128:2138-40. 2008
  5. doi request reprint Mechanisms of mutation formation with long-wave ultraviolet light (UVA)
    Thomas M Rünger
    Department of Dermatology, Boston University School of Medicine, Boston, MA 02118, USA
    Photodermatol Photoimmunol Photomed 24:2-10. 2008
  6. ncbi request reprint How different wavelengths of the ultraviolet spectrum contribute to skin carcinogenesis: the role of cellular damage responses
    Thomas M Rünger
    Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    J Invest Dermatol 127:2103-5. 2007
  7. ncbi request reprint Role of cathepsin K in the turnover of the dermal extracellular matrix during scar formation
    Thomas M Rünger
    Department of Dermatology, Boston University Medical School, Boston, Massachusetts 02467, USA
    J Invest Dermatol 127:293-7. 2007
  8. ncbi request reprint Alterations of DNA repair in melanoma cell lines resistant to cisplatin, fotemustine, or etoposide
    T M Rünger
    Department of Dermatology, Georg August University, Gottingen, Germany
    J Invest Dermatol 114:34-9. 2000
  9. ncbi request reprint DNA damage formation, DNA repair, and survival after exposure of DNA repair-proficient and nucleotide excision repair-deficient human lymphoblasts to UVA1 and UVB
    T M Rünger
    Department of Dermatology, Georg August University Gottingen, Germany
    Int J Radiat Biol 76:789-97. 2000
  10. ncbi request reprint Reduced joining of DNA ends correlates with chromosomal instability in three melanoma cell lines
    Thomas M Rünger
    Department of Dermatology, Boston University School of Medicine, Boston, MA 02118, USA
    Tumour Biol 24:100-8. 2003

Collaborators

Detail Information

Publications26

  1. doi request reprint Much remains to be learned about how UVR induces mutations
    Thomas M Rünger
    Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts 02118, USA USA
    J Invest Dermatol 133:1717-9. 2013
    ..This important information gap is filled by Ikehata et al. in this issue. Their findings question several aspects of our current thinking about UV-induced mutagenesis and carcinogenesis...
  2. doi request reprint Morphea-like skin reactions in patients treated with the cathepsin K inhibitor balicatib
    Thomas M Rünger
    Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    J Am Acad Dermatol 66:e89-96. 2012
    ..In a multicenter clinical trial in North America and Europe that tested the cathepsin K (catK) inhibitor balicatib for the treatment of osteoporosis, several patients developed hardening of the skin...
  3. doi request reprint Comparison of DNA damage responses following equimutagenic doses of UVA and UVB: a less effective cell cycle arrest with UVA may render UVA-induced pyrimidine dimers more mutagenic than UVB-induced ones
    Thomas M Rünger
    Boston University School of Medicine, Department of Dermatology, 609 Albany Street, Boston, MA 02118, USA
    Photochem Photobiol Sci 11:207-15. 2012
    ..Our data suggest that less effective anti-mutagenic cellular responses, in particular different and shorter-lived cell cycle arrests, render pyrimidine dimers induced by UVA more mutagenic than pyrimidine dimers induced by UVB...
  4. ncbi request reprint C-->T transition mutations are not solely UVB-signature mutations, because they are also generated by UVA
    Thomas M Rünger
    Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts, USA
    J Invest Dermatol 128:2138-40. 2008
    ..We hypothesize that weaker anti-mutagenic cellular responses to UVA, as compared to UVB, may result in higher rates of mutation formation for UVA-induced dimers...
  5. doi request reprint Mechanisms of mutation formation with long-wave ultraviolet light (UVA)
    Thomas M Rünger
    Department of Dermatology, Boston University School of Medicine, Boston, MA 02118, USA
    Photodermatol Photoimmunol Photomed 24:2-10. 2008
    ..We hypothesize that a weaker anti-mutagenic cellular response, but not a different type of DNA damage, may be responsible for a higher mutation rate per DNA photoproduct with UVA, as compared with UVB...
  6. ncbi request reprint How different wavelengths of the ultraviolet spectrum contribute to skin carcinogenesis: the role of cellular damage responses
    Thomas M Rünger
    Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    J Invest Dermatol 127:2103-5. 2007
    ..in this issue, may be a mechanism by which UVA augments UVB-mediated mutation and skin cancer formation...
  7. ncbi request reprint Role of cathepsin K in the turnover of the dermal extracellular matrix during scar formation
    Thomas M Rünger
    Department of Dermatology, Boston University Medical School, Boston, Massachusetts 02467, USA
    J Invest Dermatol 127:293-7. 2007
    ....
  8. ncbi request reprint Alterations of DNA repair in melanoma cell lines resistant to cisplatin, fotemustine, or etoposide
    T M Rünger
    Department of Dermatology, Georg August University, Gottingen, Germany
    J Invest Dermatol 114:34-9. 2000
    ....
  9. ncbi request reprint DNA damage formation, DNA repair, and survival after exposure of DNA repair-proficient and nucleotide excision repair-deficient human lymphoblasts to UVA1 and UVB
    T M Rünger
    Department of Dermatology, Georg August University Gottingen, Germany
    Int J Radiat Biol 76:789-97. 2000
    ..The goal of the work presented here was to further characterize the nature of UV-induced comets and to further elucidate DNA damage formation by different wavelengths of ultraviolet light...
  10. ncbi request reprint Reduced joining of DNA ends correlates with chromosomal instability in three melanoma cell lines
    Thomas M Rünger
    Department of Dermatology, Boston University School of Medicine, Boston, MA 02118, USA
    Tumour Biol 24:100-8. 2003
    ..Although a small sample was studied, this raises the possibility that defects in DNA end joining may also contribute to genetic instability and chromosome aberrations in melanoma...
  11. ncbi request reprint How disruption of cell cycle regulating genes might predispose to sun-induced skin cancer
    Thomas M Rünger
    Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Cell Cycle 4:643-5. 2005
    ..Differences in the apoptotic response to ultraviolet light between melanocytes and keratinocytes might explain why INK4a/ARF mutations predispose to malignant melanoma, but not to keratinocyte-derived skin cancers...
  12. ncbi request reprint Expression and regulation of cathepsin K in skin fibroblasts
    Maria J Quintanilla-Dieck
    Department of Dermatology, Boston University School of Medicine, Boston, MA 02118, USA
    Exp Dermatol 18:596-602. 2009
    ....
  13. ncbi request reprint Impaired processing of DNA photoproducts and ultraviolet hypermutability with loss of p16INK4a or p19ARF
    Papri Sarkar-Agrawal
    Department of Dermatology, Boston University School of Medicine, Boston, MA 02118, USA
    J Natl Cancer Inst 96:1790-3. 2004
    ..These results may further explain why INK4a/ARF mutations predispose to malignant melanoma, a UV-induced tumor...
  14. ncbi request reprint Short- and long-wave UV light (UVB and UVA) induce similar mutations in human skin cells
    Ulrike P Kappes
    Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    J Invest Dermatol 126:667-75. 2006
    ..Differences in the cellular response to UVA and UVB, such as the less prominent activation of p53 by UVA, might determine a different mutagenic outcome of UVA- and UVB-induced dimers...
  15. ncbi request reprint Cathepsin K in melanoma invasion
    Maria J Quintanilla-Dieck
    Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    J Invest Dermatol 128:2281-8. 2008
    ..Clinical use of catK inhibitors, a class of medication currently in clinical trials for the treatment of osteoporosis, may be a promising avenue for the treatment of melanoma...
  16. ncbi request reprint Activation of the Fanconi anemia/BRCA pathway and recombination repair in the cellular response to solar ultraviolet light
    Jessica Dunn
    Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Cancer Res 66:11140-7. 2006
    ....
  17. doi request reprint No formation of DNA double-strand breaks and no activation of recombination repair with UVA
    Jennifer L Rizzo
    Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    J Invest Dermatol 131:1139-48. 2011
    ..The lack of sufficient evidence for formation of DNA DSBs underlines the pivotal role of UVA-induced DNA photoproducts in UVA mutagenesis and carcinogenesis...
  18. doi request reprint Intracellular degradation of elastin by cathepsin K in skin fibroblasts--a possible role in photoaging
    Katerine A Codriansky
    Department of Dermatology, Boston University School of Medicine, Boston, MA, USA
    Photochem Photobiol 85:1356-63. 2009
    ....
  19. ncbi request reprint Modulation of base excision repair alters cellular sensitivity to UVA1 but not to UVB1
    Katherine J Kim
    Department of Dermatology, Boston University School of Medicine, MA 02118, USA
    Photochem Photobiol 75:507-12. 2002
    ..These results indicate that DNA damage, in particular oxidative DNA damage, contributes to cellular UVA1 sensitivity and underline a pivotal role of its repair in the cellular responses to UVA1...
  20. pmc Telomeric DNA induces p53-dependent reactive oxygen species and protects against oxidative damage
    Margaret S Lee
    Department of Dermatology, Boston University School of Medicine, Boston, MA 02118, USA
    J Dermatol Sci 56:154-62. 2009
    ..Telomere homolog oligonucleotides (T-oligos) induce adaptive DNA damage responses including increased DNA repair capacity and these effects are mediated, at least in part, through p53...
  21. ncbi request reprint No major role for 7,8-dihydro-8-oxoguanine in ultraviolet light-induced mutagenesis
    Ulrike P Kappes
    Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Radiat Res 164:440-5. 2005
    ..This indicates that 8-oxoG, which is processed by OGG1, does not contribute significantly to either UVA- or UVB-light-induced mutagenesis...
  22. ncbi request reprint Recurrent hemolysis-associated pseudoerysipelas of the lower legs in a patient with congenital spherocytosis
    Martin Leverkus
    Department of Dermatology, University of Wurzburg, Germany
    J Am Acad Dermatol 51:1019-23. 2004
    ..These eruptions might be caused by intermittent hemolysis-induced inflammation as a result of the increased osmotic fragility of the erythrocytes and may evolve to chronic leg ulcers later in life...
  23. doi request reprint Longwave UV light induces the aging-associated progerin
    Hirotaka Takeuchi
    Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts, USA
    J Invest Dermatol 133:1857-62. 2013
    ..These data suggest a previously unreported pathway of photoaging and support the concept that photoaging is at least in part a process of damage-accelerated intrinsic aging...
  24. doi request reprint Multicentric reticulohistiocytosis: a systemic osteoclastic disease?
    Katerine A Codriansky
    Boston University Medical Center, Boston, Massachusetts, USA
    Arthritis Rheum 59:444-8. 2008
  25. ncbi request reprint Syndromes with genetic instability: model diseases for (skin) cancerogenesis
    Steffen Emmert
    Department of Dermatology and Venereology, Georg August University, Gottingen, Germany
    J Dtsch Dermatol Ges 4:721-31. 2006
    ..They significantly contribute to our understanding of the molecular mechanisms of (skin) carcinogenesis and for the development of preventive and therapeutic anticancer strategies...
  26. doi request reprint Primary cutaneous CD56 positive lymphoma: a diagnostic conundrum in an unusual case of lymphoma
    Stefan M Schieke
    Department of Dermatology, Boston University School of Medicine, Boston, MA 02118, USA
    J Cutan Pathol 39:540-4. 2012
    ....