H Willers

Summary

Affiliation: Massachusetts General Hospital
Country: USA

Publications

  1. ncbi request reprint Distinct mechanisms of nonhomologous end joining in the repair of site-directed chromosomal breaks with noncomplementary and complementary ends
    H Willers
    Laboratory of Molecular and Cellular Radiation Biology, Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    Radiat Res 166:567-74. 2006
  2. ncbi request reprint Introduction to clinical radiation biology
    Henning Willers
    Department of Radiation Oncology, Harvard Medical School Massachusetts General Hospital, Cox 3, 55 Fruit Street, Boston, MA 02114, USA
    Hematol Oncol Clin North Am 20:1-24. 2006
  3. ncbi request reprint Homologous recombination in extrachromosomal plasmid substrates is not suppressed by p53
    H Willers
    Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    Carcinogenesis 22:1757-63. 2001
  4. pmc Deficiency of human BRCA2 leads to impaired homologous recombination but maintains normal nonhomologous end joining
    F Xia
    Laboratory of Molecular and Cellular Radiation Biology, Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA
    Proc Natl Acad Sci U S A 98:8644-9. 2001
  5. pmc Repair of radiation damage to DNA
    H Willers
    Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, 100 Blossom Street, Boston, MA 02114, USA
    Br J Cancer 90:1297-301. 2004
  6. ncbi request reprint Nonhomologous end-joining of site-specific but not of radiation-induced DNA double-strand breaks is reduced in the presence of wild-type p53
    Jochen Dahm-Daphi
    Laboratory of Experimental Radiation Oncology, Department of Radiotherapy and Radiation Oncology, University Hospital Eppendorf, University of Hamburg, 20246 Hamburg, Germany
    Oncogene 24:1663-72. 2005
  7. pmc Biomarkers and mechanisms of FANCD2 function
    Henning Willers
    Laboratory of Cellular and Molecular Radiation Oncology, Department of Radiation Oncology, Massachusetts General Hospital, Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA
    J Biomed Biotechnol 2008:821529. 2008
  8. pmc Distinct roles of XRCC4 and Ku80 in non-homologous end-joining of endonuclease- and ionizing radiation-induced DNA double-strand breaks
    Leonie Schulte-Uentrop
    Laboratory of Radiobiology and Experimental Radiation Oncology, Department of Radiotherapy and Radiation Oncology, University Medical School Hamburg Eppendorf, Martinistrasse 52, D 20246 Hamburg, Germany
    Nucleic Acids Res 36:2561-9. 2008
  9. ncbi request reprint Checkpoint kinase 2-mediated phosphorylation of BRCA1 regulates the fidelity of nonhomologous end-joining
    Jing Zhuang
    Department of Radiation Oncology, Vanderbilt University Medical Centre, 1301 22nd Avenue South, Nashville, TN 37232, USA
    Cancer Res 66:1401-8. 2006
  10. pmc Chk2 phosphorylation of BRCA1 regulates DNA double-strand break repair
    Junran Zhang
    Department of Radiation Oncology, Massachusetts General Hospital Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA
    Mol Cell Biol 24:708-18. 2004

Collaborators

  • J Dahm-Daphi
  • G Iliakis
  • Simon N Powell
  • Hong Wang
  • Junran Zhang
  • Leonie Schulte-Uentrop
  • Wael Y Mansour
  • Jing Zhuang
  • Jay H Chung
  • Fen Xia
  • Herman D Suit
  • F Xia
  • Tim Rhein
  • Fruszina Gatzemeier
  • Kerstin Borgmann
  • Sabine Schumacher
  • Raafat A El-Awady
  • Friedrich Haag
  • Lena Schliecker
  • Filip Schmidt-Petersen
  • Raphael Rosskopf
  • Dik C van Gent
  • Dennis E Hallahan
  • Jagadish C Ghosh
  • David T Weaver
  • Sang Kim
  • Zhihui Feng
  • Z C Zeng
  • D G Taghian
  • J S DeFrank

Detail Information

Publications12

  1. ncbi request reprint Distinct mechanisms of nonhomologous end joining in the repair of site-directed chromosomal breaks with noncomplementary and complementary ends
    H Willers
    Laboratory of Molecular and Cellular Radiation Biology, Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    Radiat Res 166:567-74. 2006
    ..Our NHEJ assay should prove a useful system to further elucidate the genetic determinants and molecular mechanisms of site-directed DSBs in living cells...
  2. ncbi request reprint Introduction to clinical radiation biology
    Henning Willers
    Department of Radiation Oncology, Harvard Medical School Massachusetts General Hospital, Cox 3, 55 Fruit Street, Boston, MA 02114, USA
    Hematol Oncol Clin North Am 20:1-24. 2006
    ....
  3. ncbi request reprint Homologous recombination in extrachromosomal plasmid substrates is not suppressed by p53
    H Willers
    Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    Carcinogenesis 22:1757-63. 2001
    ..These data may serve as a cautionary note for future investigations using solely extrachromosomal model systems to address DNA repair in intact cells...
  4. pmc Deficiency of human BRCA2 leads to impaired homologous recombination but maintains normal nonhomologous end joining
    F Xia
    Laboratory of Molecular and Cellular Radiation Biology, Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA
    Proc Natl Acad Sci U S A 98:8644-9. 2001
    ..Thus, there exists a specific regulation of HR by BRCA2, which may function to maintain genomic integrity and suppress tumor development in proliferating cells...
  5. pmc Repair of radiation damage to DNA
    H Willers
    Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, 100 Blossom Street, Boston, MA 02114, USA
    Br J Cancer 90:1297-301. 2004
    ....
  6. ncbi request reprint Nonhomologous end-joining of site-specific but not of radiation-induced DNA double-strand breaks is reduced in the presence of wild-type p53
    Jochen Dahm-Daphi
    Laboratory of Experimental Radiation Oncology, Department of Radiotherapy and Radiation Oncology, University Hospital Eppendorf, University of Hamburg, 20246 Hamburg, Germany
    Oncogene 24:1663-72. 2005
    ..In conclusion, our data suggest that p53 restricts the mutagenic effects of NHEJ without compromising repair proficiency or cell survival, thereby maintaining genomic stability...
  7. pmc Biomarkers and mechanisms of FANCD2 function
    Henning Willers
    Laboratory of Cellular and Molecular Radiation Oncology, Department of Radiation Oncology, Massachusetts General Hospital, Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA
    J Biomed Biotechnol 2008:821529. 2008
    ..Our data emphasize the need for multiple biomarkers, such as gammaH2AX, FANCD2, and RAD51, to capture all pathway activities...
  8. pmc Distinct roles of XRCC4 and Ku80 in non-homologous end-joining of endonuclease- and ionizing radiation-induced DNA double-strand breaks
    Leonie Schulte-Uentrop
    Laboratory of Radiobiology and Experimental Radiation Oncology, Department of Radiotherapy and Radiation Oncology, University Medical School Hamburg Eppendorf, Martinistrasse 52, D 20246 Hamburg, Germany
    Nucleic Acids Res 36:2561-9. 2008
    ..Thus, I-SceI-induced breaks may resemble DSBs arising during normal DNA metabolism and mouse development. The removal of these breaks likely has different genetic requirements than the repair of radiation-induced DSBs...
  9. ncbi request reprint Checkpoint kinase 2-mediated phosphorylation of BRCA1 regulates the fidelity of nonhomologous end-joining
    Jing Zhuang
    Department of Radiation Oncology, Vanderbilt University Medical Centre, 1301 22nd Avenue South, Nashville, TN 37232, USA
    Cancer Res 66:1401-8. 2006
    ..We suggest that the differential control of NHEJ subprocesses by BRCA1, in concert with Chk2, reduces the mutagenic potential of NHEJ, thereby contributing to the prevention of familial breast cancers...
  10. pmc Chk2 phosphorylation of BRCA1 regulates DNA double-strand break repair
    Junran Zhang
    Department of Radiation Oncology, Massachusetts General Hospital Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA
    Mol Cell Biol 24:708-18. 2004
    ..We propose a dual regulatory role for BRCA1 in maintaining genome integrity, whereby BRCA1 phosphorylation status controls the selectivity of repair events dictated by HR and error-prone NHR...
  11. ncbi request reprint Comment on "Tumor response to radiotherapy regulated by endothelial cell apoptosis" (I)
    Herman D Suit
    Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA
    Science 302:1894; author reply 1894. 2003
  12. pmc Hierarchy of nonhomologous end-joining, single-strand annealing and gene conversion at site-directed DNA double-strand breaks
    Wael Y Mansour
    Laboratory of Radiobiology and Experimental Radiation Oncology, Department of Radiotherapy and Radiation Oncology, University Medical School Hamburg Eppendorf, Martinistrasse 52, D 20246 Hamburg, Germany
    Nucleic Acids Res 36:4088-98. 2008
    ..Furthermore, the cellular choice of repair pathways is reversible and can be influenced at the level of effector proteins such as Ku80 or Rad51...