Seminars in Radiation Oncology
Volume 13, Issue 1 , Pages 13-21 , January 2003

The mechanism of action of radiosensitization of conventional chemotherapeutic agents

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    Effect of radiation on thymidine phosphorylase levels in HT29 human colon cancer cells. HT29 cells were irradiated with 4 Gy. They were assessed for up to 18 days later for thymidine phosphorylase con

    Effect of radiation on thymidine phosphorylase levels in HT29 human colon cancer cells. HT29 cells were irradiated with 4 Gy. They were assessed for up to 18 days later for thymidine phosphorylase content by immunoblotting.

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    Gemcitabine-mediated radiosensitization of ribonucleotide reductase overexpressing cells. Cells transduced with the active M2 subunit (showing increased activity of ribonucleotide reductase) and the i

    Gemcitabine-mediated radiosensitization of ribonucleotide reductase overexpressing cells. Cells transduced with the active M2 subunit (showing increased activity of ribonucleotide reductase) and the inactive M1 subunit (as a control) were the kind gift of Y Yen. Cells were treated with gemcitabine for 24 hours before irradiation. They were then assessed for clonogenic survival.

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    Effect of MLH1 mutation and mismatch repair defect on cytotoxicity and radiosensitization of HCT-116 human colon cancer cells. HCT-116 cells were obtained from the American Type Culture Collection. HC

    Effect of MLH1 mutation and mismatch repair defect on cytotoxicity and radiosensitization of HCT-116 human colon cancer cells. HCT-116 cells were obtained from the American Type Culture Collection. HCT-116 cells containing chromosome 3 (mismatch repair competent) or chromosome 2 (mismatch repair defective, as are the parental cells, as a control for containing an extra chromosome) were exposed to the indicated concentrations of drug for 24 hours. They were then were assessed for clonogenic survival (left) or for radiation sensitivity (right). Radiation sensitivity is expressed as the ratio of the mean inactivation dose (area under the cell survival curve) of the control divided by that of the drug-treated cells.

 Address reprint requests to Theodore S. Lawrence, MD, PhD, University of Michigan, Department of Radiation Oncology, 1500 E Medical Center Drive, B2C502 UH, Ann Arbor, MI 48109-0010.

PII: S1053-4296(03)50004-2

doi: 10.1053/srao.2003.50002

Seminars in Radiation Oncology
Volume 13, Issue 1 , Pages 13-21 , January 2003