OBJECTIVES Expression of prostaglandin biosynthetic pathway enzymes in mucinous pancreatic cysts is unknown. Cyclooxygenase-2 (COX-2) inhibition is a potential cancer chemoprevention strategy for these lesions. We evaluated the expression of COX-2, cytosolic phospholipase A2 (cPLA2), and protein kinase B (AKT) in the epithelium of pancreatic cysts and correlated enzyme expression with aspirin (ASA) use and cyst fluid prostaglandin E2 (PGE2) concentration. METHODS Pathology of 80 resected pancreatic cysts was reviewed. Expression of COX-2, cPLA2, and AKT was quantified by tissue immunohistochemistry immunoreactivity scores (IRSs). IRS values were compared between cyst types and (in 30 cases) with matched cyst fluid PGE2 concentrations. RESULTS The mean IRS was higher in the epithelium of mucinous vs nonmucinous cysts for COX-2 (6.1 ± 4.7 vs 3.2 ± 2.8, P = 0.01) and cPLA2 (6.9 ± 3.0 vs 2.9 ± 2.9, P < 0.001). Cyst epithelial COX-2 expression was higher in mucinous cysts with low-grade dysplasia vs those with high-grade dysplasia or invasive carcinoma (IRS 8.0 ± 3.9 vs 1.5 ± 2.9, P < 0.001), whereas the opposite was found for cPLA2 (6.2 ± 3.0 vs 8.6 ± 2.3, P = 0.005). Cyst fluid PGE2 concentrations did not correlate with either the IRS or a history of low- to moderate-dose ASA use. CONCLUSIONS COX-2 and cPLA2 are overexpressed in the epithelium of mucinous pancreatic cysts. COX-2 and/or cPLA2 inhibition might prevent the emergence or progression of mucinous pancreatic cysts, but higher doses of ASA or nonsteroidal anti-inflammatory drugs may be necessary to substantially inhibit cyst epithelial COX-2 activity.

中文翻译：

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Cyclooxygenase-2和胞质磷脂酶A2在粘液性胰腺囊肿中过表达。

目的粘液性胰腺囊肿中前列腺素生物合成途径酶的表达尚不清楚。环氧合酶2（COX-2）抑制是针对这些病变的潜在癌症化学预防策略。我们评估了胰腺囊肿上皮中COX-2，胞质磷脂酶A2（cPLA2）和蛋白激酶B（AKT）的表达，并评估了阿司匹林（ASA）使用和囊液前列腺素E2（PGE2）浓度与酶表达的相关性。方法回顾性分析80例切除的胰腺囊肿的病理。通过组织免疫组织化学免疫反应评分（IRS）量化COX-2，cPLA2和AKT的表达。比较了囊肿类型与（30例）囊肿液中PGE2浓度匹配的IRS值。结果COX-2的粘液性囊肿与非粘液性囊肿上皮中的平均IRS较高（6.1±4.7 vs 3。2±2.8，P = 0.01）和cPLA2（6.9±3.0 vs 2.9±2.9，P <0.001）。低度不典型增生的粘液囊肿的囊肿上皮COX-2表达高于高度不典型增生或浸润性癌的囊肿（IRS 8.0±3.9 vs 1.5±2.9，P <0.001），而cPLA2则相反（6.2 ±3.0与8.6±2.3，P = 0.005）。囊肿液中PGE2的浓度与IRS或低至中等剂量ASA的使用史均无关。结论COX-2和cPLA2在粘液性胰腺囊肿的上皮细胞中过表达。抑制COX-2和/或cPLA2可能会阻止粘液性胰腺囊肿的出现或进展，但可能需要更高剂量的ASA或非甾体类抗炎药才能充分抑制囊肿上皮COX-2活性。低度不典型增生的粘液囊肿的囊肿上皮COX-2表达高于高度不典型增生或浸润性癌的囊肿（IRS 8.0±3.9 vs 1.5±2.9，P <0.001），而cPLA2则相反（6.2 ±3.0与8.6±2.3，P = 0.005）。囊肿液中PGE2的浓度与IRS或低至中等剂量ASA的使用史均无关。结论COX-2和cPLA2在粘液性胰腺囊肿的上皮细胞中过表达。抑制COX-2和/或cPLA2可能会阻止粘液性胰腺囊肿的出现或进展，但可能需要更高剂量的ASA或非甾体类抗炎药才能充分抑制囊肿上皮COX-2活性。低度不典型增生的粘液囊肿的囊肿上皮COX-2表达高于高度不典型增生或浸润性癌的囊肿（IRS 8.0±3.9 vs 1.5±2.9，P <0.001），而cPLA2则相反（6.2 ±3.0与8.6±2.3，P = 0.005）。囊肿液中PGE2的浓度与IRS或低至中剂量ASA的使用史均无关。结论COX-2和cPLA2在粘液性胰腺囊肿的上皮细胞中过表达。抑制COX-2和/或cPLA2可能会阻止粘液性胰腺囊肿的出现或进展，但可能需要更高剂量的ASA或非甾体类抗炎药才能充分抑制囊肿上皮COX-2活性。0±3.9对1.5±2.9，P <0.001），而cPLA2则相反（6.2±3.0对8.6±2.3，P = 0.005）。囊肿液中PGE2的浓度与IRS或低至中等剂量ASA的使用史均无关。结论COX-2和cPLA2在粘液性胰腺囊肿的上皮细胞中过表达。抑制COX-2和/或cPLA2可能会阻止粘液性胰腺囊肿的出现或进展，但可能需要更高剂量的ASA或非甾体类抗炎药才能充分抑制囊肿上皮COX-2活性。0±3.9对1.5±2.9，P <0.001），而cPLA2则相反（6.2±3.0对8.6±2.3，P = 0.005）。囊肿液中PGE2的浓度与IRS或低至中等剂量ASA的使用史均无关。结论COX-2和cPLA2在粘液性胰腺囊肿的上皮细胞中过表达。抑制COX-2和/或cPLA2可能会阻止粘液性胰腺囊肿的出现或进展，但可能需要更高剂量的ASA或非甾体类抗炎药才能充分抑制囊肿上皮COX-2活性。结论COX-2和cPLA2在粘液性胰腺囊肿的上皮细胞中过表达。抑制COX-2和/或cPLA2可能会阻止粘液性胰腺囊肿的出现或进展，但可能需要更高剂量的ASA或非甾体类抗炎药才能充分抑制囊肿上皮COX-2活性。结论COX-2和cPLA2在粘液性胰腺囊肿的上皮细胞中过表达。抑制COX-2和/或cPLA2可能会阻止粘液性胰腺囊肿的出现或进展，但可能需要更高剂量的ASA或非甾体类抗炎药才能充分抑制囊肿上皮COX-2活性。