Residual γH2AX foci predict local tumour control after radiotherapy.

[1]  M. Krause,et al.  GTV differentially impacts locoregional control of non-small cell lung cancer (NSCLC) after different fractionation schedules: subgroup analysis of the prospective randomized CHARTWEL trial. , 2013, Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology.

[2]  K. Ang,et al.  Management of human papillomavirus-positive and human papillomavirus-negative head and neck cancer. , 2012, Seminars in radiation oncology.

[3]  Mechthild Krause,et al.  Individualization of cancer treatment from radiotherapy perspective , 2012, Molecular oncology.

[4]  M. Krause,et al.  Residual DNA double strand breaks in perfused but not in unperfused areas determine different radiosensitivity of tumours. , 2011, Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology.

[5]  M. Baumann,et al.  Radiobiological hypoxia, histological parameters of tumour microenvironment and local tumour control after fractionated irradiation. , 2010, Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology.

[6]  B. Beuthien-Baumann,et al.  Prediction of clonogenic cell survival curves based on the number of residual DNA double strand breaks measured by γH2AX staining , 2009, International journal of radiation biology.

[7]  C. Aquino-Parsons,et al.  γH2AX Expression in Tumors Exposed to Cisplatin and Fractionated Irradiation , 2009, Clinical Cancer Research.

[8]  P. Olive,et al.  Kinetics of H2AX phosphorylation after exposure to cisplatin , 2009, Cytometry. Part B, Clinical cytometry.

[9]  M. Krause,et al.  The extreme radiosensitivity of the squamous cell carcinoma SKX is due to a defect in double-strand break repair. , 2009, Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology.

[10]  K. Trott,et al.  Cancer stem cells and radiotherapy , 2009, International journal of radiation biology.

[11]  Yves Pommier,et al.  γH2AX and cancer , 2008, Nature Reviews Cancer.

[12]  George Iliakis,et al.  γ-H2AX in recognition and signaling of DNA double-strand breaks in the context of chromatin , 2008, Nucleic acids research.

[13]  T. Misteli,et al.  Activation of the Cellular DNA Damage Response in the Absence of DNA Lesions , 2008, Science.

[14]  K. Eckardt,et al.  Upregulation of hypoxia-inducible factors in normal and psoriatic skin. , 2007, The Journal of investigative dermatology.

[15]  T. Helleday,et al.  DNA double-strand break repair: from mechanistic understanding to cancer treatment. , 2007, DNA repair.

[16]  Danny Vesprini,et al.  Homologous recombination and prostate cancer: a model for novel DNA repair targets and therapies. , 2007, Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology.

[17]  M. Krause,et al.  Pre-treatment number of clonogenic cells and their radiosensitivity are major determinants of local tumour control after fractionated irradiation. , 2007, Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology.

[18]  R. Mirzayans,et al.  Relationship between DNA double-strand break rejoining and cell survival after exposure to ionizing radiation in human fibroblast strains with differing ATM/p53 status: implications for evaluation of clinical radiosensitivity. , 2006, International journal of radiation oncology, biology, physics.

[19]  M. Krause,et al.  Pimonidazole labelling and response to fractionated irradiation of five human squamous cell carcinoma (hSCC) lines in nude mice: the need for a multivariate approach in biomarker studies. , 2006, Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology.

[20]  Takeo Ohnishi,et al.  Does γH2AX foci formation depend on the presence of DNA double strand breaks , 2005 .

[21]  K. McManus,et al.  ATM-dependent DNA damage-independent mitotic phosphorylation of H2AX in normally growing mammalian cells. , 2005, Molecular biology of the cell.

[22]  Michael Baumann,et al.  Molecular markers predicting radiotherapy response: report and recommendations from an International Atomic Energy Agency technical meeting. , 2005, International journal of radiation oncology, biology, physics.

[23]  M. Krause,et al.  Does heterogeneity of pimonidazole labelling correspond to the heterogeneity of radiation-response of FaDu human squamous cell carcinoma? , 2005, Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology.

[24]  J. Bussink,et al.  Thymidine analogues to assess microperfusion in human tumors. , 2005, International journal of radiation oncology, biology, physics.

[25]  P. Olive,et al.  Radiation Sensitivity, H2AX Phosphorylation, and Kinetics of Repair of DNA Strand Breaks in Irradiated Cervical Cancer Cell Lines , 2004, Cancer Research.

[26]  P. Olive,et al.  Phosphorylated Histone H2AX in Spheroids, Tumors, and Tissues of Mice Exposed to Etoposide and 3-Amino-1,2,4-Benzotriazine-1,3-Dioxide , 2004, Cancer Research.

[27]  P. Olive,et al.  Phosphorylation of histone H2AX as a measure of radiosensitivity. , 2004, International journal of radiation oncology, biology, physics.

[28]  P. Olive,et al.  Expression of phosphorylated histone H2AX as a surrogate of cell killing by drugs that create DNA double-strand breaks. , 2003, Cancer research.

[29]  Kai Rothkamm,et al.  Pathways of DNA Double-Strand Break Repair during the Mammalian Cell Cycle , 2003, Molecular and Cellular Biology.

[30]  Ying-li Yu,et al.  Cell Cycle-Dependent Expression of Phosphorylated Histone H2AX: Reduced Expression in Unirradiated but not X-Irradiated G1-Phase Cells , 2003, Radiation research.

[31]  P. Olive,et al.  Expression of phosphorylated histone H2AX in cultured cell lines following exposure to X‐rays , 2003, International journal of radiation biology.

[32]  Kai Rothkamm,et al.  Evidence for a lack of DNA double-strand break repair in human cells exposed to very low x-ray doses , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[33]  E. Rogakou,et al.  Megabase Chromatin Domains Involved in DNA Double-Strand Breaks in Vivo , 1999, The Journal of cell biology.

[34]  E. Rogakou,et al.  DNA Double-stranded Breaks Induce Histone H2AX Phosphorylation on Serine 139* , 1998, The Journal of Biological Chemistry.

[35]  L. M. Cobb,et al.  Distribution of pimonidazole and RSU 1069 in tumour and normal tissues. , 1990, British Journal of Cancer.

[36]  M. Baumann,et al.  Response of human squamous cell carcinoma xenografts of different sizes to irradiation: relationship of clonogenic cells, cellular radiation sensitivity in vivo, and tumor rescuing units. , 1990, Radiation research.

[37]  T. Dörk,et al.  Aberrant overexpression of miR-421 downregulates ATM and leads to a pronounced DSB repair defect and clinical hypersensitivity in SKX squamous cell carcinoma. , 2013, Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology.

[38]  C. Aquino-Parsons,et al.  Endogenous and radiation-induced expression of gammaH2AX in biopsies from patients treated for carcinoma of the uterine cervix. , 2010, Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology.

[39]  H D Suit,et al.  Clinical interest in determinations of cellular radiation sensitivity. , 1989, International journal of radiation biology.