DNA Damage and Repair of Head and Neck Cancer Cells after Radio- and Chemotherapy

2009 ◽  
Vol 64 (7-8) ◽  
pp. 601-610 ◽  
Author(s):  
Pawel Rusin ◽  
Anna Walczak ◽  
Anita Zwierzchlejska ◽  
Jurek Olszewski ◽  
Alina Morawiec-Bajda ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Head And Neck Cancer ◽  
Head And Neck ◽  
Cancer Cells ◽  
Neck Cancer ◽  
Cancer Cell Line ◽  
Repair Capacity ◽  
Dna Damage And Repair ◽  
Γ Radiation

DNA repair is critical for successful chemo- and radiotherapy of human tumours, because their genotoxic sensitivity may vary in different types of cancer cells. In this study we have compared DNA damage and the efficiency of its repair after genotoxic treatment with hydrogen peroxide, cisplatin and γ-radiation of head and neck squamous cell carcinoma (HNSCC). Lymphocytes and tissue cells from biopsies of 37 cancer patients and 35 healthy donors as well as the HTB-43 larynx cancer cell line were employed. The cell sensitivity to genotoxic treatment was estimated by the MTT survival assay. The extent of DNA damage and efficiency of its repair was examined by the alkaline comet assay. Among the examined treatments, we found that HNSCC cells were the most sensitive to γ-radiation and displayed impaired DNA repair. In particular, DNA damage was repaired less effectively in cells from HNSCC metastasis than healthy controls. In conclusion, our results suggest that the different genotoxic sensitivity of HNSCC cells may depend on their DNA repair capacity what in turn may be connected with the effectiveness of head and neck cancer therapy.

scholarly journals Targeting of β1 integrins impairs DNA repair for radiosensitization of head and neck cancer cells

Oncogene ◽  
2015 ◽  
Vol 35 (11) ◽  
pp. 1353-1362 ◽  
Author(s):  
E Dickreuter ◽  
I Eke ◽  
M Krause ◽  
K Borgmann ◽  
M A van Vugt ◽  
...  
Keyword(s):  
Dna Repair ◽  
Head And Neck Cancer ◽  
Head And Neck ◽  
Cancer Cells ◽  
Neck Cancer ◽  
Β1 Integrins

scholarly journals DNA Repair Capacity and the Risk of Head and Neck Cancer

10.5772/31555 ◽  
2012 ◽  
Author(s):  
Marcin Szaumkessel ◽  
Wojciech Gawcki ◽  
Krzysztof Szyfter
Keyword(s):  
Dna Repair ◽  
Head And Neck Cancer ◽  
Head And Neck ◽  
Neck Cancer ◽  
Repair Capacity ◽  
Dna Repair Capacity

Comparative study of DNA damage and repair in head and neck cancer after radiation treatment

2009 ◽  
Vol 33 (3) ◽  
pp. 357-363 ◽  
Author(s):  
Pawel Rusin ◽  
Jurek Olszewski ◽  
Alina Morawiec-Bajda ◽  
Karolina Przybylowska ◽  
Dariusz Kaczmarczyk ◽  
...  
Keyword(s):  
Dna Damage ◽  
Head And Neck Cancer ◽  
Comparative Study ◽  
Head And Neck ◽  
Neck Cancer ◽  
Radiation Treatment ◽  
Dna Damage And Repair

scholarly journals DNA damage and repair in lymphocytes of normal individuals and cancer patients: studies by the comet assay and micronucleus tests.

2003 ◽  
Vol 50 (1) ◽  
pp. 181-190 ◽  
Author(s):  
Olena Palyvoda ◽  
Joanna Polańska ◽  
Andrzej Wygoda ◽  
Joanna Rzeszowska-Wolny
Keyword(s):  
Dna Damage ◽  
Head And Neck Cancer ◽  
Comet Assay ◽  
Cancer Patient ◽  
Head And Neck ◽  
Patient Group ◽  
Neck Cancer ◽  
Dna Damage And Repair ◽  
Damage Level ◽  
Healthy Donors

A population study is reported in which the DNA damage induced by g-radiation (2 Gy) and the kinetics of the subsequent repair were estimated by the comet and micronucleus assays in isolated lymphocytes of 82 healthy donors and patients with head and neck cancer before radiotherapy. The parameters of background and radiation-induced DNA damage, rate of repair, and residual non-repaired damage were measured by comet assay, and the repair kinetics for every donor were computer-fitted to an exponential curve. The level of background DNA damage before irradiation measured by comet assay as well as the level of micronuclei were significantly higher in the head and neck cancer patient group than in the healthy donors, while the parameters of repair were widely scattered in both groups. Cancer patient group contained significantly more individuals, whose irradiated lymphocytes showed high DNA damage, low repair rate and high non-repaired DNA damage level. Lymphocytes of donors belonging to this subgroup showed significantly lower inhibition of cell cycle after irradiation.

scholarly journals Synergistic Cytotoxicity From Combination of Lupeol and Ionizing Radiation in Head and Neck Cancer Cells.

2021 ◽  
Author(s):  
Sayantan Bhattacharyya ◽  
Paramita Ghosh ◽  
Depanwita Saha ◽  
Debarpan Mitra ◽  
Samir Banerjee ◽  
...  
Keyword(s):  
Head And Neck Cancer ◽  
Ionizing Radiation ◽  
Synergistic Effect ◽  
Head And Neck ◽  
Cancer Cells ◽  
Neck Cancer ◽  
Combination Treatment ◽  
Short Interval ◽  
Cancer Cell Line ◽  
Synergistic Cytotoxicity

Abstract Ionizing radiation (IR) is one of the most conventional treatment regimens for treatment of Head and Neck Squamous Cell Carcinoma (HNSCC). It is often employed as a primary treatment or as an adjuvant to surgery. Despondently IR has its own drawbacks including radiation resistance, poor prognosis and frequent recurrence. The main objective of this work was to check the synergistic effect of Lupeol along with IR in order to observe if adjuvant treatment of novel phytochemicals like Lupeol with IR shows better efficacy. Head and Neck cancer cell line HEp-2 and UPCI: SCC 131 was treated with both Lupeol (50 µM) and IR (2 Gy) for short interval and the cytotoxicity of the drug combination was evaluated. Data showed synergistic effect of Lupeol with IR in both cell lines. The combination of lupeol and IR had highest cytotoxicity, induction of apoptosis was also found to be higher in the combination treatment. Additionally the combination also inhibited cell migration and sphere formation capability indicating direct effect of the combinatorial treatment on the Epithelial to Messenchymal transition (EMT) forming population of HNSCC cells. Findings also showed downregulation of key oncoproteins (AKT, NF-kB, COX-2) in the combination treatment proving synergistic effect of Lupeol with ionizing radiation in killing Head and Neck cancer cells by downregulating several oncogenic pathways.

scholarly journals 498 Improving Surgical and Non-Surgical Oncological Outcomes in Patients with Head and Neck Cancer

2021 ◽  
Vol 108 (Supplement_6) ◽  
Author(s):  
B Atkinson ◽  
J Wilson
Keyword(s):  
Dna Repair ◽  
Head And Neck Cancer ◽  
Side Effects ◽  
Head And Neck ◽  
Neck Cancer ◽  
Cancer Cell Line ◽  
Mild Hyperthermia ◽  
Squamous Cells ◽  
Intensity Score ◽  
Dna Repair Protein

Abstract Introduction Treatment of head and neck cancer is complex and involves a multi-disciplinary approach between surgeons and oncologists. Radiotherapy often leaves patients with debilitating side effects such as mucositis, sialadenitis and dysphagia. Radiation induces double strand breaks (DSBs) in DNA within both normal squamous cells and squamous cell carcinomas (SCCs) that, if left unrepaired, initiates programmed cell death. Like normal squamous cells, SCC’s have an effective DNA repair pathway to protect against apoptosis by repairing DSBs through proteins such as FanD2-S331. This study aims to show that mild hyperthermia inhibits FancD2, therefore having the potential to increase the susceptibility of SCCs to radiotherapy and subsequently reducing the side effects. Method Head and neck cancer cell line UMSCC47 was cultured, then irradiated with 2 Gray before washing with an anti γH2AX antibody, used as a biomarker for DSBs. Fluorescent antibodies against FacD2-S331 were then used to assess the levels present within the nucleus of cells exposed to mild hyperthermia (39 °C) and then compared to untreated cells and cells exposed to radiation only. Results A γH2AX fluorophore intensity score of 58 following radiation compared to 20 in the control confirmed the presence of DSBs. A FancD2-s331 fluorophore intensity score of 76 was observed in cells exposed radiation. Cells exposed to heat prior to radiation showed a FancD2-s331 fluorophore score of 21. Conclusions Exposure of SCCs to mild hyperthermia before radiotherapy reduces activation of DNA repair protein FancD2-S2331. A reduction in DNA repair increases the susceptibility of SCCs to radiotherapy and apoptosis.

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