Cyclooxygenase-2 (Cox-2) Expression in Lymphomas

Hazar, Burhan; Ergïn, Melek; Seyrek, E.; Erdoğan, Şeyda; Tuncer, İlhan; Hakverdı, Sibel

doi:10.1080/10428190310001654032

Cited by 43 publications

(41 citation statements)

References 22 publications

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“…In a small study, Hazar et al demonstrated that in 70% of Hodgkin's patients' HRS cells expressed Cox-2 [32]. Another study showed that HRS cells from nearly half of patients screened expressed Cox-2 and this was associated with increased proliferation and malignant cell survival [3].…”

Section: Hodgkin's Lymphomamentioning

confidence: 99%

“…More recent studies have shown that patients whose lymphomas expressed Cox-2 were more likely to have aggressive tumor growth. In one study, 57% of patients expressed Cox-2 in their non-Hodgkin's lymphoma cells [32]. Cox-2 expression was determined through immunohistochemical analysis and was further correlated with poor response to chemotherapy.…”

Section: Non-hodgkin's Lymphomamentioning

confidence: 99%

See 1 more Smart Citation

Targeting Cyclooxygenase-2 in Hematological Malignancies: Rationale and Promise

Bernard¹,

Bancos²,

Sime³

et al. 2008

CPD

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There is much interest in the potential use of Cox-2 selective inhibitors in combination with other cancer therapeutics. Malignancies of hematopoietic and non-hematopoietic origin often have increased expression of cyclooxygenase-2 (Cox-2), a key modulator of inflammation. For example, hematological malignancies such as chronic lymphocytic leukemia, chronic myeloid leukemia, Hodgkin's lymphoma, non-Hodgkin's lymphoma and multiple myeloma often highly express Cox-2, which correlates with poor patient prognosis. Expression of Cox-2 enhances survival and proliferation of malignant cells, while negatively influencing anti-tumor immunity. Hematological malignancies expressing elevated levels of Cox-2 potentially avoid immune responses by producing factors that enhance angiogenesis and metastases. Cellular immune responses regulated by natural killer cells, cytotoxic T lymphocytes, and T regulatory cells are also influenced by Cox-2 expression. Therefore, Cox-2 selective inhibitors have promising therapeutic potential in patients suffering from certain hematological malignancies.

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Section: Hodgkin's Lymphomamentioning

confidence: 99%

Section: Non-hodgkin's Lymphomamentioning

confidence: 99%

Targeting Cyclooxygenase-2 in Hematological Malignancies: Rationale and Promise

Bernard¹,

Bancos²,

Sime³

et al. 2008

CPD

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“…Several cytokines, chemokines and inflammatory enzymes are known to induce COX-2 expression. [53][54][55] The data analysis presented above for COX-2 staining intensity show for the first time that COX-2 expression can independently predict prostate cancer recurrence. The sensitivity, specificity and accuracy of COX-2 staining to predict biochemical recurrence Note that 62 months, 72 months and 100 months were used as a cut point for determining biochemical recurrence.…”

Section: Determination Of Sensitivity Specificity Accuracy Ppv Andmentioning

confidence: 99%

“…For example, in non-Hodgkin's lymphoma, high COX-2 expression correlates with increased stage, lower survival and lower complete response rate to therapy. 55 In breast cancer, COX-2 overexpression occurs in 43% of human invasive breast cancers and 63% of ductal carcinomas in situ. 57,58 Furthermore, high expression of COX-2 associates with decreased disease specific survival.…”

Section: Determination Of Sensitivity Specificity Accuracy Ppv Andmentioning

confidence: 99%

Cyclooxygenase‐2 (cox‐2) expression is an independent predictor of prostate cancer recurrence

Cohen

Gómez

Omori

et al. 2006

Intl Journal of Cancer

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Lack of reliable prognostic markers hinders accurate prediction of disease progression in prostate cancer. The inducible proinflammatory enzyme cyclooxygenase-2 (COX-2) is implicated in prostate carcinogenesis, but its role in cancer progression is less clear. We examined whether COX-2 expression evaluated by immunohistochemistry (IHC) in radical prostatectomy (RP) specimens can predict biochemical recurrence. Archival prostate cancer specimens (n 5 60) were obtained from patients who underwent RP, but had not received neoadjuvant hormonal therapy. Twentythree patients had biochemical or clinical recurrence (mean time of recurrence: 38.2 months), and 37 patients were recurrence free (mean follow-up: 95 months). COX-2 expression was determined by IHC, using an anti-COX-2 antibody. Three individuals scored the staining independently, as high-or low-expression. COX-2 was expressed in prostate cancer cells, in adjacent normal glands and in specimens from patients who later progressed. At 62-months follow-up, COX-2 staining predicted progression with 82.4% sensitivity and 81.3% specificity. Sensitivity (86.4%) and specificity (86.7%) improved at 100-months follow-up. In univariate analysis, Gleason score, preoperative PSA, extraprostatic extension, margin, seminal vesicle invasion, and high COX-2 expression were significant predictors of biochemical recurrence (p < 0.05). In multivariate analysis, preoperative PSA (hazard ratio/unit PSA change 1.080; p 5 0.0036) and COX-2 expression (hazard ratio 16.442; p < 0.0001) were independent prognostic indicators. Patients with PSA > 7 ng/ml and high COX-2 expression had the highest probability of recurrence (Kaplan-Meier analysis). COX-2 expression is an independent predictor of prostate cancer progression following RP and underscores the significance of inflammatory factors in this process. ' 2006 Wiley-Liss, Inc.Key words: inflammation; immunohistochemistry; PSA; cancer progression; prognostic indicators; multivariate analysis; tumor markers Cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) are prostaglandin endoperoxide synthases, which are rate limiting enzymes in the conversion of the fatty acid arachidonic acid into physiologically active eicosanoids such as prostaglandin, thromboxane and prostacyclin. 1 COX-2 is the inducible form of COX that is frequently elevated in cancer tissues. [2][3][4] Although the mechanism of COX-2 action in carcinogenesis or progression is not well established, COX-2 inhibitors have been shown to be chemopreventive in cancer, specifically in colorectal cancer. [5][6][7] The expression and role of COX-2 in prostate cancer has been a topic of several reports over the decade. 8,9 There exists some controversy over the expression, detection and the putative role of COX-2 in prostate carcinogenesis and progression. While early studies reported high-level expression of COX-2 in prostate, findings from subsequent studies have been mixed. [10][11][12] Typically, later studies reported low or no expression in normal, benign prostatic hyperplasi...

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“…A recent study also demonstrated that patients with Hp + early-stage DLBCL could achieve complete pathological remission via Hp eradication (22). Studies have found that there is a clinical correlation between COX-2 expression and prognostic factors in lymphoma patients (23)(24)(25), and that IL-32 is also closely linked with T-cell lymphoma and Hp + gastritis (12,26). However, the expression of COX -2 and IL-32, …”

Section: Discussionmentioning

confidence: 99%

Expression and clinical significance of cyclooxygenase-2 and interleukin-32 in primary gastric B-cell lymphoma

Cui

Sun

et al. 2015

Oncology Letters

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Abstract. Cyclooxygenase-2 (COX-2) and interleukin-32 (IL-32) expression has been examined in various carcinomas and inflammations, and has been suggested to be significant in tumor progression and prognosis. The present study was conducted to investigate the expression of COX-2 and IL-32 in primary gastric B-cell lymphoma in order to define their clinical significance and their association with Helicobacter pylori (Hp) infection. COX-2 and IL-32 protein expression was detected in 31 primary gastric B-cell lymphoma patients and 19 chronic gastritis patients with immunohistochemistry. COX-2 and IL-32 expression was significantly higher in primary gastric lymphoma (PGL) tissues compared with gastritis tissues (51.6 vs. 21.1% for COX-2, P= 0.032; and 58.1 vs. 26.3% for IL-32, P= 0.029) and was significantly higher in Hp + lymphoma tissues compared with Hp -lymphoma tissues (66.7 vs. 20% for COX-2, P= 0.015; and 71.4 vs. 30% for IL-32, P= 0.029). In the PGL tissues, the expression level of COX-2 was positively correlated with the expression level of IL-32, and the two were each positively correlated with Hp infection (P= 0.004 for COX-2 and IL-32; P= 0.01 for COX-2 and Hp infection; and P= 0.003 for IL-32 and Hp infection). COX-2 expression was found to be significantly associated (P<0.05) with an aggressive tumor type, higher expression of Ki-67, frequent lymph node metastasis and advanced stage. IL-32 expression was found to be significantly correlated (P<0.05) with frequent lymph node metastasis and an advanced stage. The survival time was longer in the COX-2 -and IL-32 -lymphoma patients compared with the COX-2 + and IL-32 + lymphoma patients, but these differences were not statistically significant. These results suggested that Hp infection and the expression of COX-2 and IL-32 were closely linked with each other, and that the overexpression of COX-2 and IL-32 was correlated with tumor progression in primary gastric B-cell lymphoma, thus indicating potential novel therapeutic target.

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Cyclooxygenase-2 (Cox-2) Expression in Lymphomas

Cited by 43 publications

References 22 publications

Targeting Cyclooxygenase-2 in Hematological Malignancies: Rationale and Promise

Targeting Cyclooxygenase-2 in Hematological Malignancies: Rationale and Promise

Cyclooxygenase‐2 (cox‐2) expression is an independent predictor of prostate cancer recurrence

Expression and clinical significance of cyclooxygenase-2 and interleukin-32 in primary gastric B-cell lymphoma

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