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Henning Willers, MD

  • Phone: 617-726-5184
Departments
Department of Radiation Oncology

Specialties

  • Cancer Center
  • Thoracic Cancers
  • Radiation Oncology
Clinical Interests
Lung cancer
Stereotactic Body Radiation Therapy (SBRT)
Proton Radiation Therapy
Molecular targeted radiation therapy
Esophageal cancer
Locations
Boston: Massachusetts General Hospital
Medical Education
MD, University of Hamburg School of Medicine
Residency, Hermann Holthusen Institute for Radiotherapy
Residency, Massachusetts General Hospital
Board Certifications
Radiation Oncology, American Board of Radiology
Gender
Male
Patient Age Group
Adult
Accepting New Patients
Yes

Research

Dr. Willers is a laboratory-based clinician-scientist in Radiation Oncology with an interest in basic, translational, and clinical lung cancer research. He is an Assistant Professor in Radiation Oncology and a Principal Investigator in the Laboratory of Cellular & Molecular Radiation Oncology in the MGH Cancer Center.

Research in Dr. Willers' laboratory evolves around the concept that the goal of cancer therapy using ionizing radiation and/or chemotherapeutic agents is to selectively kill cancer cells while sparing surrounding normal tissues. In order to achieve this, pre-existing genetic differences between tumors and normal tissues have to be exploited. To this end, the laboratory has two main research interests: (i) To detect and characterize altered DNA repair in cancer that may render the affected tumors hypersensitive to DNA damaging agents. (ii) To identify and disrupt altered signal transduction pathways, which may sensitize tumors to radiation. For both of these approaches, predictive tests need to be established to guide the identification of patients with the highest likelihood of benefiting from novel treatment regimens. Dr. Willers' long-term goal is to contribute to the realization of "personalized" or "individualized" cancer therapy.

Publications

Selected from a total of 36 peer-reviewed publications:

Willers H, et al. High-dose radiation therapy alone for inoperable non-small cell lung cancer-experience with prolonged overall treatment times. Acta Oncol. 1998;37(1):101-5

Willers H, et al. Dissociation of p53-mediated suppression of homologous recombination from G1/S cell cycle checkpoint control. Oncogene. 2000;19(5):632-9.

Willers H, Held KD. Introduction to clinical radiation biology. Hemat Oncol Clin N. America 2006;20:1-24.

Schulte-Uentrop L, et al. Distinct roles of XRCC4 and Ku80 in non-homologous end-joining of endonuclease- and ionizing radiation-induced DNA double-strand breaks. Nucleic Acids Res. 2008; 36:2561-9.

Nanda A, et al. Unusual tumor response and toxicity from radiation and concurrent erlotinib for non-small cell lung cancer. Clin Lung Cancer 2008; 9:285-87.

Willers H, et al. Utility of DNA repair protein foci for the detection of putative BRCA1-pathway defects in breast cancer biopsies. Mol. Cancer Res. 2009; 7(8):1304-9.

Clark Center for Radiation Oncology
100 Blossom Street
Boston, MA 02114-2606

Phone: 617-726-5184
Fax: 617-726-3603

Radiation Oncology- Boston Medical Center
830 Harrison Avenue
Boston, MA 02118

Phone: 617-726-5184
Fax: 617-726-3603

Clark Center for Radiation Oncology
100 Blossom Street
Boston, MA 02114-2606

Phone: 617-726-5184
Fax: 617-726-3603

Radiation Oncology- Boston Medical Center
830 Harrison Avenue
Boston, MA 02118

Phone: 617-726-5184
Fax: 617-726-3603

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