ABSTRACT
BACKGROUND: While it is well known that cyclooxygenase-2 (COX-2) expression is increased in colorectal adenoma and carcinoma, there is only limited information on its status in stromal tumours. METHODS: Immunohistochemical COX-2 staining was performed on a total of 42 confirmed gastrointestinal stromal tumours (GISTs) in the Pathology Department of Gaziantep University and the findings were compared with various other parameters. RESULTS: We found a statistically significant correlation between the tumor mitosis and COX-2 expression in GISTs. However, there was no relationship between COX-2 expression and death rate, presence of metastasis, tumour size, risk staging, usage of tyrosine kinase inhibitors, and complete resection rate. CONCLUSIONS: In the light of these findings, the usage of COX-2 inhibitors with or without tyrosine kinase inhibitors in GIST patients may be helpful in the adjuvant setting to prevent or delay recurrence. Moreover, we need more studies to define the status of COX-2 inhibitors in GISTs.
Subject(s)
Cyclooxygenase 2/metabolism , Gastrointestinal Stromal Tumors/metabolism , Gastrointestinal Stromal Tumors/pathology , Mitosis , Adult , Aged , Antineoplastic Agents/therapeutic use , Benzamides , Chi-Square Distribution , Cyclooxygenase 2 Inhibitors/therapeutic use , Disease Progression , Female , Gastrointestinal Stromal Tumors/drug therapy , Gastrointestinal Stromal Tumors/mortality , Gastrointestinal Stromal Tumors/surgery , Humans , Imatinib Mesylate , Immunohistochemistry , Indoles/therapeutic use , Male , Middle Aged , Neoplasm Metastasis , Piperazines/therapeutic use , Protein-Tyrosine Kinases/antagonists & inhibitors , Pyrimidines/therapeutic use , Pyrroles/therapeutic use , Retrospective Studies , Sunitinib , Survival Rate , Tumor BurdenABSTRACT
OBJECTIVE: To investigate the protective effect of antibiotherapy in the early phase of acute pancreatitis on cellular injury induced in lungs and liver. BACKGROUND: Cellular viability and plasma nitric oxide (NO) levels were assessed to determine the efficacy of highly bactericidal imipenem and quinolones on liver and lung injury. METHODS: Imipenem, levofloxacin or saline were administered to rats with caerulein induced pancreatitis. Twenty-four hours later serum amylase, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, and NO levels, pancreatic interstitial inflammation, acinar cell necrosis, acinar cell vacuolisation, peripancreatic fat necrosis; spotty necrosis, focal inflammation of liver and inflammatory processes in the lungs were assessed. RESULTS: Enzyme levels in the antibiotherapy groups were lower than in the control group. Serum NO levels were higher only in the imipenem group. Levofloxacin decreased acinar cell vacuolisation in the pancreas; interstitial edema, neutrophilic infiltration and interstitial enlargement in the lungs. Antibiotherapy decreased spotty necrosis, apoptosis and focal inflammation in the liver. CONCLUSIONS: Although treatment with imipenem is associated with higher NO levels than levofloxacin, levofloxacin prevents organ injury more effectively than imipenem in acute pancreatitis. Our results indicate that antibiotherapy in the early period of necrotizing pancreatitis prevents cellular damage induced in pancreas, liver and lungs.
