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Improving Gemcitabine-Mediated Radiosensitization Using Molecularly Targeted Therapy: A Review

Authors' Affiliations: Departments of ¹ Radiation Oncology, and ² Pharmacology, University of Michigan, Ann Arbor, Michigan

Requests for reprints: Meredith A. Morgan, Department of Radiation Oncology, University of Michigan Medical Center, 1301 Catherine Street, Room 4326A Medical Sciences I, Ann Arbor, MI 48109-5637. Phone: 734-647-5928; Fax: 734-763-1581; E-mail: mmccrack{at}med.umich.edu.

In the last three decades, gemcitabine has progressed from the status of a laboratory cytotoxic drug to a standard clinical chemotherapeutic agent and a potent radiation sensitizer. In an effort to improve the efficacy of gemcitabine, additional chemotherapeutic agents have been combined with gemcitabine (both with and without radiation) but with toxicity proving to be a major limitation. Therefore, the integration of molecularly targeted agents, which potentially produce less toxicity than standard chemotherapy, with gemcitabine radiation is a promising strategy for improving chemoradiation. Two of the most promising targets, described in this review, for improving the efficacy of gemcitabine radiation are epidermal growth factor receptor and checkpoint kinase 1.