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Dual PI3K/mTOR Inhibitor NVP-BEZ235 Leads to a Synergistic Enhancement of Cisplatin and Radiation in Both HPV-Negative and -Positive HNSCC Cell Lines
2022 - Forschungsinformationssystem des UKE - frei zugänglich
Establishment of a Transformation Coupled in vitro End Joining Assay to Estimate Radiosensitivity in Tumor Cells
2020 - Forschungsinformationssystem des UKE
Dual PI3K/mTOR Inhibitor NVP-BEZ235 Enhances Radiosensitivity of Head and Neck Squamous Cell Carcinoma (HNSCC) Cell Lines Due to Suppressed Double-Strand Break (DSB) Repair by Non-Homologous End Joining
2020 - Forschungsinformationssystem des UKE
HPV-positive HNSCC cell lines show strongly enhanced radiosensitivity after photon but not after carbon ion irradiation
2020 - Forschungsinformationssystem des UKE
In HPV-Positive HNSCC Cells, Functional Restoration of the p53/p21 Pathway by Proteasome Inhibitor Bortezomib Does Not Affect Radio- or Chemosensitivity
2019 - Forschungsinformationssystem des UKE - frei zugänglich
HPV-negative and HPV-positive HNSCC cell lines show similar numerical but different structural chromosomal aberrations
2019 - Forschungsinformationssystem des UKE
BCL2-overexpressing prostate cancer cells rely on PARP1-dependent end-joining and are sensitive to combined PARP inhibitor and radiation therapy
2018 - Forschungsinformationssystem des UKE
Roscovitine strongly enhances the effect of olaparib on radiosensitivity for HPV neg. but not for HPV pos. HNSCC cell lines
2017 - Forschungsinformationssystem des UKE
Radiation DNA damage and use in cancer/therapeutics-translation of radiation modifiers
2016 - Forschungsinformationssystem des UKE
Impaired 53BP1/RIF1 DSB mediated end-protection stimulates CtIP-dependent end resection and switches the repair to PARP1-dependent end joining in G1
2016 - Forschungsinformationssystem des UKE
Functional crosstalk between DNA damage response proteins 53BP1 and BRCA1 regulates double strand break repair choice
2016 - Forschungsinformationssystem des UKE
Cancer cell motility is affected through 3D cell culturing and SCF/c-Kit pathway but not by X-irradiation
2016 - Forschungsinformationssystem des UKE
Sorafenib inhibits cell growth but fails to enhance radio- and chemosensitivity of glioblastoma cell lines
2016 - Forschungsinformationssystem des UKE
DNA repair after oncological therapy (radiotherapy and chemotherapy)
2016 - Forschungsinformationssystem des UKE
Loss of CHD1 causes DNA repair defects and enhances prostate cancer therapeutic responsiveness
2016 - Forschungsinformationssystem des UKE
Quantitative proteomics unveiled: Regulation of DNA double strand break repair by EGFR involves PARP1
2015 - Forschungsinformationssystem des UKE
EGFRvIII does not affect radiosensitivity with or without gefitinib treatment in glioblastoma cells
2015 - Forschungsinformationssystem des UKE
Association between SNPs in defined functional pathways and risk of early or late toxicity as well as individual radiosensitivity
2015 - Forschungsinformationssystem des UKE
Inhibition of PARP1-dependent end-joining contributes to Olaparib-mediated radiosensitization in tumor cells
2014 - Forschungsinformationssystem des UKE - frei zugänglich
The inhibition of PARP but not EGFR results in the radiosensitization of HPV/p16-positive HNSCC cell lines
2014 - Forschungsinformationssystem des UKE

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Dual PI3K/mTOR Inhibitor NVP-BEZ235 Leads to a Synergistic Enhancement of Cisplatin and Radiation in Both HPV-Negative and -Positive HNSCC Cell Lines

Establishment of a Transformation Coupled in vitro End Joining Assay to Estimate Radiosensitivity in Tumor Cells

Dual PI3K/mTOR Inhibitor NVP-BEZ235 Enhances Radiosensitivity of Head and Neck Squamous Cell Carcinoma (HNSCC) Cell Lines Due to Suppressed Double-Strand Break (DSB) Repair by Non-Homologous End Joining

HPV-positive HNSCC cell lines show strongly enhanced radiosensitivity after photon but not after carbon ion irradiation

In HPV-Positive HNSCC Cells, Functional Restoration of the p53/p21 Pathway by Proteasome Inhibitor Bortezomib Does Not Affect Radio- or Chemosensitivity

HPV-negative and HPV-positive HNSCC cell lines show similar numerical but different structural chromosomal aberrations

BCL2-overexpressing prostate cancer cells rely on PARP1-dependent end-joining and are sensitive to combined PARP inhibitor and radiation therapy

Roscovitine strongly enhances the effect of olaparib on radiosensitivity for HPV neg. but not for HPV pos. HNSCC cell lines

Radiation DNA damage and use in cancer/therapeutics-translation of radiation modifiers

Impaired 53BP1/RIF1 DSB mediated end-protection stimulates CtIP-dependent end resection and switches the repair to PARP1-dependent end joining in G1

Functional crosstalk between DNA damage response proteins 53BP1 and BRCA1 regulates double strand break repair choice

Cancer cell motility is affected through 3D cell culturing and SCF/c-Kit pathway but not by X-irradiation

Sorafenib inhibits cell growth but fails to enhance radio- and chemosensitivity of glioblastoma cell lines

DNA repair after oncological therapy (radiotherapy and chemotherapy)

Loss of CHD1 causes DNA repair defects and enhances prostate cancer therapeutic responsiveness

Quantitative proteomics unveiled: Regulation of DNA double strand break repair by EGFR involves PARP1

EGFRvIII does not affect radiosensitivity with or without gefitinib treatment in glioblastoma cells

Association between SNPs in defined functional pathways and risk of early or late toxicity as well as individual radiosensitivity

Inhibition of PARP1-dependent end-joining contributes to Olaparib-mediated radiosensitization in tumor cells

The inhibition of PARP but not EGFR results in the radiosensitization of HPV/p16-positive HNSCC cell lines