Increased Prostaglandin E Production in Malignant Lymphomas

Sébahoun, G; Maraninchi, D; Carcassonne, Y

doi:10.1159/000206188

Cited by 7 publications

(3 citation statements)

References 9 publications

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“…There is an expanding need for new therapies to combat the various types of non-Hodgkin's lymphomas. Early investigation revealed that a majority of non-Hodgkin's lymphoma patients, as well as Hodgkin's lymphoma patients had elevated levels of plasma PGE 2 , however, at the time no clinical correlation was made [34]. More recent studies have shown that patients whose lymphomas expressed Cox-2 were more likely to have aggressive tumor growth.…”

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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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: 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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“…Consequently, strategies that circumvent resistance to TRAIL-mediated apoptosis may further enhance its activity in human lymphoma, in particular, new drugs targeting tumor microenvironment itself or blocking the crosstalk between tumor microenvironment and lymphoma B cells. High levels of PGE 2 have been found in the plasma of patients with lymphoma (24) and recent studies have revealed that patients with DLBCL also exhibit high COX-2 expression (25).…”

Section: Introductionmentioning

confidence: 99%

COX-2–Independent Effects of Celecoxib Sensitize Lymphoma B Cells to TRAIL-Mediated Apoptosis

Gallouët

Travert

Bresson

et al. 2014

Clinical Cancer Research

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Purpose: Despite therapeutic advances, non-Hodgkin lymphomas (NHL) remain incurable. They form a group of neoplasms strongly dependent on their inflammatory microenvironment, which plays an important supportive role in tumor B-cell survival and in the resistance to antitumor immune response. New therapies must consider both tumor cells and their surrounding microenvironment Experimental Design: Stromal cells, derived from bone marrow or lymph nodes, and B cells from follicular lymphoma patients were cocultured or cultured alone with celecoxib treatment, a nonsteroidal anti-inflammatory drug, and/or TRAIL, a promising cytotoxic molecule for cancer therapy.Results: In this study, we show that follicular lymphoma stromal cells produce large amounts of PGE 2 . This production is abrogated after celecoxib treatment, targeting the COX-2 isoenzyme involved in PGE 2 synthesis. Furthermore, we demonstrate that celecoxib increases apoptosis in NHL B-cell lines and in primary follicular lymphoma B cells cocultured with stromal cells, but independently of the PGE 2 /COX-2 axis. Finally, celecoxib increases the apoptotic activity of TRAIL. We provide evidence that celecoxib affects proliferation and sensitizes NHL B-cell lines to apoptosis through COX-2-independent effects by slowing down the cell cycle and decreasing the expression of survival proteins, such as Mcl-1.Conclusions: These data suggest new potent strategies for NHL therapy combining drugs targeting both tumor B cells and survival signals provided by the tumor microenvironment.

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“…6,[12][13][14][15] Although the role of COX-2 in lymphoid carcinogenesis is poorly defined, high levels of prostaglandins have been found in patients with lymphoma, and elevated levels of COX-2 protein have been detected in lymphoma cell lines. 16,17 Microarray technology has been previously used to profile gene expression in B-CLL and to subcharacterize patients with heterogeneous clinical outcome. 18 -23 Because it has been clearly shown that B-CLL cells are defective in their apoptotic response, in searching for new potential therapeutic targets, we have analyzed by cDNA microarray the expression profile of a set of stressand toxicity-associated genes, including COX-2/PTGS2, in B-CLL samples in comparison with normal B lymphocytes.…”

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confidence: 99%