Premium
Immunohistochemical analysis of cyclooxygenase (COX)‐2 expression in pancreatic endocrine tumors: Association with tumor progression and proliferation
Author(s) -
Ohike Nobuyuki,
Morohoshi Toshio
Publication year - 2001
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1046/j.1440-1827.2001.01273.x
Subject(s) - immunohistochemistry , pathology , ki 67 , malignancy , pathological , pleomorphism (cytology) , vasoactive intestinal peptide , medicine , gastrin , receptor , neuropeptide , secretion
An immunohistochemical study of cyclooxygenase (COX)‐2 expression in pancreatic endocrine tumors (PET) was carried out, and the expression of COX‐2 was compared with pathological features, the expression of several markers (hormones, vascular endothelial growth factor, single‐stranded DNA, and the Ki‐67 labeling index [LI]). Twenty PET, including 10 metastasizing cases (tumor size: 3–8 cm) and 10 non‐metastasizing cases (tumor size: 0.3– 8 cm) were studied. Tumors with a high level of COX‐2 expression were placed in the H group, and the remaining tumors were placed in the L group. The H group was comprised of 13 tumors: all 10 of the metastasizing cases and three of the non‐metastasizing cases. There were significant differences in tumor size between the two groups (H group 46.5 mm; L group 0.9 mm). There were significant differences in the presence of the following histological criteria for malignancy: pleomorphism (H group 13/13; L group 1/7), mitotic activity (H group 2.9; L group 0) and/or angioinvasion (H group 13/13; L group 1/7); and there were also significant differences in the number of cases that expressed ectopic hormones (gastrin, vasoactive intestinal peptide, serotonin and calcitonin; H group 12/13; L group 2/7) and in the Ki‐67 LI (H group 8.3%; L group 0.4%). The distribution of COX‐2‐positive cells tended to be similar to the distribution of Ki‐67‐positive cells. Our data show that COX‐2 is frequently upregulated in malignant PET and that there is a close relationship between COX‐2 expression and tumor progression / proliferative activity.