Radiation Resistance in a Doxorubicin-Resistant Human Fibrosarcoma Cell Line
| Autor: | Patrick R. Miller, Marilyn L. Slovak, Anna B. Hill, David S. Shimm |
|---|---|
| Rok vydání: | 1992 |
| Předmět: |
Cancer Research
Pathology medicine.medical_specialty Cell Survival DNA damage Fibrosarcoma medicine.medical_treatment Drug Resistance Drug resistance Radiation Tolerance Radioresistance Tumor Cells Cultured medicine Humans Radiation resistance Chemotherapy business.industry Cell Cycle Dose-Response Relationship Radiation Flow Cytometry medicine.disease Radiation therapy Oncology Doxorubicin Cancer research HT1080 business |
| Zdroj: | American Journal of Clinical Oncology. 15:216-221 |
| ISSN: | 0277-3732 |
| DOI: | 10.1097/00000421-199206000-00007 |
| Popis: | In clinical practice, cancers refractory to chemotherapy can appear relatively radioresistant. Recent work in multidrug-resistant cell lines has yielded conflicting results concerning the relationship between drug resistance and radiation resistance. The current study examines the radiation response of a human fibrosarcoma (HT1080) and a doxorubicin-resistant subline (HT1080/DR4). Using soft-agar colony formation after graded doses of x-rays as an endpoint, HT1080/DR4 had an increased D0 (D0 = 2.1 Gy) and a broader initial shoulder (n = 2.7, Dq = 2.1 Gy) than the parental HT1080 line (D0 = 0.7, Gy, n = 1.2, Dq = 0.3 Gy), suggesting that HT1080/DR4 has an increased capacity to repair radiation-induced DNA damage. This possibility was tested by comparing the cell lines' ability to accumulate sublethal damage. In split-dose recovery experiments, HT1080/DR4 demonstrated increased ability to repair sublethal radiation damage following fractionated irradiation, compared with the HT1080 parental line. The mechanism for this radiation resistance is not clear, but a variety of cellular alterations seen in drug-resistant cell lines are discussed with reference to areas of further study. |
| Databáze: | OpenAIRE |
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