Tara M. Breslin, Nora A. Janjan, Jeffrey E. Lee, Peter W. T. Pisters, Robert A. Wolff, James L. Abbruzzese, Douglas B. Evans

Pancreatic Tumor Study Group: Departments of Surgical Oncology (TMB, JEL, PWTP, DBE), Radiation Oncology (NAJ), and Gastrointestinal Oncology and Digestive Diseases (RAW, JLA), The University of Texas M. D. Anderson Cancer Center, Houston, TX

Received 6/4/98 Accepted 5/5/98

8. PERSPECTIVE

The future of multimodality therapy for patients with potentially resectable adenocarcinoma of the pancreas depends on the development of treatment schemas which emphasize minimizing toxicity, and treatment duration, while attempting to improve therapeutic efficacy. New, more potent radiation-sensitizing agents enhance cytotoxicity and maximize local control. Systemic therapies will be directed at specific molecular events involved in pancreatic tumorigenesis (i.e., inhibition of angiogenesis, the use of protease inhibitors [matrix metalloproteinase inhibitors], or inhibition of ras-dependent signal transduction (Figure 7). These agents should be of low toxicity to permit administration during the preoperative period as well as prolonged postoperative administration.

Figure 7. The future of multimodality therapy for patients with potentially resectable adenocarcinoma of the pancreatic head. Treatment schemas emphasize the importance of minimizing toxicity, and treatment duration, while attempting to improve therapeutic efficacy. Cytotoxicity is enhanced by combining radiation therapy with more potent radiation-sensitizing agents. Systemic therapy is continued after both chemoradiation and surgery with systemic agents of low toxicity directed at specific molecular events involved in pancreatic tumorigenesis (i.e., inhibition of angiogenesis, the use of protease inhibitors [matrix metalloproteinase inhibitors], inhibition of ras-dependent signal transduction, or strategies for the use of gene therapy). Abbreviations: EB-IORT, electron-beam intraoperative radiation therapy.