Journal
LEUKEMIA
Volume 24, Issue 6, Pages 1179-1185Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/leu.2010.66
Keywords
COX-2; prostaglandin; CTCL; diagnosis; proliferation
Categories
Funding
- Danish Research Councils
- Danish Cancer Society (Kraeftens Bekaempelse)
- Lundbeck Foundation
- Novo Nordic Foundation
- AP Moller Foundation for the Advancement of Medical Science (Fonden til Laegevidenskabenskabene Fremme)
- Neye Foundation (Neye Fonden)
- Danish Foundation for Advanced Technology (Hojteknologifonden)
- Beckett Foundation (Beckett Fonden)
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Cancer often originates from a site of persistent inflammation, and the mechanisms turning chronic inflammation into a driving force of carcinogenesis are intensely investigated. Cyclooxygenase-2 (COX-2) is an inducible key modulator of inflammation that carries out the rate-limiting step in prostaglandin synthesis. Aberrant COX-2 expression and prostaglandin E-2 (PGE(2)) production have been implicated in tumorigenesis. In this study we show that COX-2 is ectopically expressed in malignant T-cell lines from patients with cutaneous T-cell lymphoma (CTCL) as well as in situ in lymphocytic cells in 21 out of 22 patients suffering from mycosis fungoides (MF) in plaque or tumor stage. COX-2 is not expressed in lymphocytes of 11 patients with patch-stage MF, whereas sporadic COX-2 staining of stromal cells is observed in the majority of patients. COX-2 expression correlates with a constitutive production of PGE(2) in malignant T cells in vitro. These cells express prostaglandin receptors EP3 and EP4 and the receptor antagonist as well as small interfering RNA (siRNA) directed against COX-2, and specific COX-2 inhibitors strongly reduce their spontaneous proliferation. In conclusion, our data indicate that COX-2 mediated PGE(2) exerts an effect as a tumor growth factor in MF. Leukemia (2010) 24, 1179-1185; doi:10.1038/leu.2010.66; published online 29 April 2010
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