Clinicopathlogical and Moleculer Studies for the Mechanism of Recurrence after Resection of Pancreatic Cancer

Daisuke Minabe

The Second Department of Surgery, Yokohama City University, School of Medicine (Director: Prof. Hiroshi Shimada)

We clarified the mechanism of recurrence after pancreatic cancer resection through clinicopathlogical and moleculer studies were attempted. The clinocopathological profiles of 25 patients who undergoing pancreatectomy for pancreatic cancerwere evaluated, using multivariate analysis. A significant prognostic factor for liver metastasis was venous invasion (v factor) in the main tumor, and that for both local recurrence and peritoneal metastasis was lymph vessel invasion (1y factor). The polymerase chain reaction (PCR) targeting the mutant K-ras gene was applied to detect cancer cells in tissue specimens from liver, peritoneum, and marrow during surgery from 13 patients with pancreatic cancer. In only 1 (25.0%) patient with v3 among the 4 patients with more than v2 who developed postoperative liver metastasis, the mutant K-ras gene was detected in liver tissue specimen. In 4 of 5 (80.0%) patients with more than 1y2, the mutant K-ras gene was detected in peritoneal tissue specimens, and all developed peritoneal recurrence. In 2 of the 4 (50.0%) with more than v2 and 1y2, the mutant K-ras gene was detected in bone marrow tissue, and all suffered distant metastasis. In conclusion, the recurrence after pancreatic cancer resection is mainly caused by micrometastasis rapidly formed by venous or lymph vessel invasion.

Key words
pancreatic cancer, recurrence, micrometastasis, mutant K-ras gene, vessel invasion

Reprint requests
Daisuke Minabe The Second Department of Surgery, Yokohama City University, School of Medicine 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004 JAPAN

Accepted
September 19, 2001

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