Cox-2 protein expression was unrelated either to the degree of dysplasia or to the size of the adenomas (p > 0.50, p > 0.10, respectively) or to differentiation, Dukes stage or lymph node metastasis of carcinomas (all p > 0.50).
COX-2 protein was overexpressed in 91 (54.8%) tumors; COX-2 overexpression was correlated with a differentiated histologic type, deep invasion, and positive lymph node metastasis.
A statistically significant association between COX-2 expression and lymph node metastasis in NPC patients, with an OR of 4.44 (95%CI = 3.46-5.70, I2 = 38.3%, Pheterogeneity = 0.024), and with other indicators of disease progression.
All the metastatic microcarcinoma tissues had increased expression levels of the two proteins in comparison with microcarcinoma tissues without lymph node metastases; however, this variation was only statistically significant for COX-2 expression levels.
As a consequence, the expression of COX-2 and PCNA was found in cancer tissues with a higher strong reactivity rate, compared with the ANCTs (80.0 vs. 53.3%, P=0.011; 68.9 vs. 48.9%, P=0.047), and COX-2 was positively associated with lymph node metastasis of GAC patients (P=0.011).
Cytoplasmic HuR expression was significantly associated with COX-2 expression (p < .025) and lymph node metastasis (p < .050) and distant metastasis (p < .025).
Expression of Cox-2 is elevated in gastric adenocarcinomas, which correlates with several clinicopathological parameters, including depth of invasion and lymph node metastasis.
Formalin-fixed paraffin-embedded tissues from 26 primary MCCs and 7 lymph node metastases were stained immunohistochemically with a monoclonal antibody directed against COX-2, and the percentage and intensity of staining were analyzed semiquantitatively.
However, COX-2 positivity did not show a statistically significant association with any other clinicopathologic characteristic (parity, body mass index, histotype, International Federation of Gynecology and Obstetrics stage, grade, lymph node metastasis, deep myometrial invasion, or p53 overexpression).
In addition, overexpression of COX-2 was found more frequently in colorectal tumors with lymphatic invasion, regional lymph node metastasis and larger size, although without statistical significance.
Interestingly, the proportion of adenocarcinoma cells with marked COX-2 expression was much greater in lymph node metastases than in the corresponding primary tumors.
Our meta-analysis demonstrates that the presence of high levels of COX-2 is associated with poor prognosis for breast cancer patients and predicts bigger tumor size and lymph node metastasis.
Overexpression of COX-2 in cancer tissues compared with matched non-cancerous tissues was found in 70% of cases and was significantly associated with lymphatic involvement, lymph node metastasis and advanced tumor stage.
Positive COX-2 expression rate was 67.76% (103/152), and its positive expression was related to FIGO stage, differentiation degree, and myometrial invasion depth of patients (P < 0.05), but not to lymph node metastasis (P > 0.05).
Results showed that COX-2 overexpression was significantly correlated with degree of differentiation (P = 0.000), and lymph node metastasis (negative/positive, P = 0.002).