Table 1.

Correlation between COX-2 level and other biomarkers found in tumoral tissues

Tissue Location and Type of Cancer	Correlation with Other Biomarkers
Colon cancer [66], primary tumors and metastatic lymph nodes resections for colorectal adenocarcinoma [93], stage II and III colorectal cancer patients [94]	High levels of COX-2 correlates with high levels of MMP-2 and VEGF expression and shorter survival time [93,94].
Cervical cancer [67]	Multivariate analysis of COX-2 levels in tumor/stromal compartments. The proportion of CD3+, CD4+, and CD25+ cells was lower in tumors with high tumor/stroma ratios, but in these tumors, mast cells were increased [67].
Ovarian cancer [95,96,97]	No correlation between COX-2 expression and EGFR, and HER-2/neu status [96].
Human breast cancer cell lines and tumors [26,98,99,100]	Elevated COX-2 expression associated with a large tumor size, a high histological grade, a negative hormone receptor status, a high proliferation rate, high p53 expression, and the presence of HER-2 oncogene amplification along with axillary node metastases and a ductal type of histology [98]. COX-2 inhibition may potentially prevent the development of ER-positive and ER-negative breast cancers [98]. Expression of PGE2 and IL-8 [101]. COX-2 over-expression induces an oncogenic microRNA (miR655) in human breast cancer cells by activation of EP4 [102].
Ductal carcinoma in situ (DCIS) [103,104,105]	COX-2 expression stabilizes survivin, an inhibitor of apoptosis (IAP) [103]. CacyBP expression was significantly negatively associated with the COX expression [104].
Non-small cell lung cancer [68,69]	Correlation between HER-2, EGFR, and COX-2 expression in patients of non-small cell lung cancer at different degrees [69]
Laryngeal cancer [71]	Cox-2 overexpression was significantly associated with radioresistant tumors [71].
Papillary thyroid cancer [106]	The expression of COX-2 is increased with age in papillary thyroid cancer [106]. Immunohistochemically, expression of COX-2 and VEGF-C correlated strongly, and both were induced by the tumor promoter phorbol 12-myristate 13-acetate [107].
Endometrial hyperplasia and carcinoma [108,109,110]	No correlation between COX-2 expression with estrogen (ER) or progesterone receptor (PR), p53, and neu [110]. Correlation between COX-2 (59%) and aromatase (65%) expression but not estrogen and progesterone receptor [111].
Invasive gallbladder cancer [112]	COX-2, c-Met, β-catenin, c-erbB2 and EGFR were over-expressed in 80%, 74%, 71%, 62%, and 11% of invasive gallbladder cancers, respectively [112].
Prostate cancer Metastatic primary prostate carcinoma compared to non-metastatic cancers [113,114,115,116]	COX-2 and Ki-67 antigen co-expression in 42.9% and 67% of the prostate cancer patients [113]. Patients with PSA > 7 ng/mL and high COX-2 expression had the highest probability of recurrence [114]. The expressions of COX-2 and E-cadherin are very firmly and inversely correlated as prognostic indicators. [115]. High expression of COX-2, TGF-beta, and Ki67 in metastatic primary prostate carcinoma was associated with death from prostate carcinoma [116].
Gastric cancer [117,118]	A positive correlation between COX-2 and K-ras expression with the depth of invasion and lymph node metastasis in gastric cancer [117]. Epithelial MMP-2 expression in gastric cancer is associated with aggressive forms, COX-2 expression, and poor survival [118].
Cervical cancer [119]	DNA hypermethylation of the COX-2 gene may be a potential prognostic marker in the early stages of cervical cancer [119].
Pancreatic cancer [120,121] Anaplastic pancreatic cancer [122]	Tumor COX-2 expression portends a poor prognosis for patients with resected adenocarcinoma of the pancreas, particularly in tumors > or = 3 cm [121]. Expression of L1CAM, COX-2, and EGFR in the majority of undifferentiated pancreatic carcinomas [122].