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21 Einträge gefunden

Src family kinase targeting in head and neck tumor cells using SU6656, PP2 and dasatinib
2023 - Forschungsinformationssystem des UKE - frei zugänglich
Impaired DNA double-strand break repair and effective radiosensitization of HPV-negative HNSCC cell lines through combined inhibition of PARP and Wee1
2023 - Forschungsinformationssystem des UKE - frei zugänglich
A Lack of Effectiveness in the ATM-Orchestrated DNA Damage Response Contributes to the DNA Repair Defect of HPV-Positive Head and Neck Cancer Cells
2022 - Forschungsinformationssystem des UKE - frei zugänglich
Dual Inhibition of PARP and the Intra-S/G2 Cell Cycle Checkpoints Results in Highly Effective Radiosensitization of HPV-Positive HNSCC Cells
2021 - Forschungsinformationssystem des UKE - frei zugänglich
Analyzing expression and phosphorylation of the EGF receptor in HNSCC
2019 - Forschungsinformationssystem des UKE - frei zugänglich
Analyzing the influence of kinase inhibitors on DNA repair by differential proteomics of chromatin-interacting proteins and nuclear phospho-proteins
2017 - Forschungsinformationssystem des UKE
G2-checkpoint targeting and radiosensitization of HPV/p16-positive HNSCC cells through the inhibition of Chk1 and Wee1
2017 - Forschungsinformationssystem des UKE
Sorafenib inhibits cell growth but fails to enhance radio- and chemosensitivity of glioblastoma cell lines
2016 - Forschungsinformationssystem des UKE
Similar cisplatin sensitivity of HPV-positive and -negative HNSCC cell lines
2016 - Forschungsinformationssystem des UKE
DNA repair after oncological therapy (radiotherapy and chemotherapy)
2016 - Forschungsinformationssystem des UKE
Radiosensitization of HNSCC cells by EGFR inhibition depends on the induction of cell cycle arrests
2016 - Forschungsinformationssystem des UKE
EGFRvIII does not affect radiosensitivity with or without gefitinib treatment in glioblastoma cells
2015 - Forschungsinformationssystem des UKE
Quantitative proteomics unveiled: Regulation of DNA double strand break repair by EGFR involves PARP1
2015 - Forschungsinformationssystem des UKE
The inhibition of PARP but not EGFR results in the radiosensitization of HPV/p16-positive HNSCC cell lines
2014 - Forschungsinformationssystem des UKE
HNSCC cell lines positive for HPV and p16 possess higher cellular radiosensitivity due to an impaired DSB repair capacity.
2013 - Forschungsinformationssystem des UKE
Sorafenib sensitizes head and neck squamous cell carcinoma cells to ionizing radiation
2013 - Forschungsinformationssystem des UKE
Inactivation of HNSCC cells by 90Y-labeled cetuximab strictly depends on the number of induced DNA double-strand breaks.
2013 - Forschungsinformationssystem des UKE
p53 modulates homologous recombination at I-SceI-induced double-strand breaks through cell-cycle regulation.
2013 - Forschungsinformationssystem des UKE
HPV-positive HNSCC cell lines but not primary human fibroblasts are radiosensitized by the inhibition of Chk1
2013 - Forschungsinformationssystem des UKE
In tumor cells regulation of DNA double strand break repair through EGF receptor involves both NHEJ and HR and is independent of p53 and K-Ras status.
2011 - Forschungsinformationssystem des UKE

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Src family kinase targeting in head and neck tumor cells using SU6656, PP2 and dasatinib

Impaired DNA double-strand break repair and effective radiosensitization of HPV-negative HNSCC cell lines through combined inhibition of PARP and Wee1

A Lack of Effectiveness in the ATM-Orchestrated DNA Damage Response Contributes to the DNA Repair Defect of HPV-Positive Head and Neck Cancer Cells

Dual Inhibition of PARP and the Intra-S/G2 Cell Cycle Checkpoints Results in Highly Effective Radiosensitization of HPV-Positive HNSCC Cells

Analyzing expression and phosphorylation of the EGF receptor in HNSCC

Analyzing the influence of kinase inhibitors on DNA repair by differential proteomics of chromatin-interacting proteins and nuclear phospho-proteins

G2-checkpoint targeting and radiosensitization of HPV/p16-positive HNSCC cells through the inhibition of Chk1 and Wee1

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

Similar cisplatin sensitivity of HPV-positive and -negative HNSCC cell lines

DNA repair after oncological therapy (radiotherapy and chemotherapy)

Radiosensitization of HNSCC cells by EGFR inhibition depends on the induction of cell cycle arrests

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

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

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

HNSCC cell lines positive for HPV and p16 possess higher cellular radiosensitivity due to an impaired DSB repair capacity.

Sorafenib sensitizes head and neck squamous cell carcinoma cells to ionizing radiation

Inactivation of HNSCC cells by 90Y-labeled cetuximab strictly depends on the number of induced DNA double-strand breaks.

p53 modulates homologous recombination at I-SceI-induced double-strand breaks through cell-cycle regulation.

HPV-positive HNSCC cell lines but not primary human fibroblasts are radiosensitized by the inhibition of Chk1

In tumor cells regulation of DNA double strand break repair through EGF receptor involves both NHEJ and HR and is independent of p53 and K-Ras status.