Larynx cancer and prostaglandins

Cenik, Ziya; Cenik, Ayse; Uyar, Yavuz

doi:10.1016/0196-0709(90)90003-e

Cited by 3 publications

(3 citation statements)

References 35 publications

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“…In several studies, serum concentrations of arachidonic acid metabolites were found to be increased in patients with head and neck cancer, and these levels decreased postoperatively 20,21 . Additionally, increased serum levels of prostaglandins were found to be associated with increased tumor stage 22,23 . With respect to arachidonic acid metabolites in tumor tissue, increased levels of these substances have been correlated with increasing stage or size of tumor.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Head and Neck Tumor Cell Growth With Arachidonic Acid Metabolism Inhibition

1996

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Head and neck tumors are known to synthesize arachidonic acid metabolites. The authors have postulated that these substances may confer growth advantage to cancer cells, and by interfering with arachidonic acid metabolism squamous cancer growth may be altered. The tongue derived squamous carcinoma cell line, SCC-25, was treated with three leukotriene synthesis inhibitors and indomethacin. A dose-dependent decrease in DNA synthesis occurred with leukotriene inhibition, but not prostaglandin inhibition. All leukotriene synthesis inhibitors produced a dramatic and immediate effect ( > 70% inhibition by 4 hours) without cytotoxicity ( > 90% trypan blue exclusion). Cell populations at 96 hours were decreased when compared to control populations. In conclusion, leukotrienes or other lipoxygenase products may play a role as growth factors for squamous cell carcinoma, and arachidonic acid inhibition may be a novel target for chemotherapeutic intervention.

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Section: Discussionmentioning

confidence: 99%

Inhibition of Head and Neck Tumor Cell Growth With Arachidonic Acid Metabolism Inhibition

1996

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“…There is emerging evidence that inhibition of PG formation can protect against these forms of cancer in animals and humans. [1][2][3][4][5][6][7][8][9][10] Prostaglandins are derived from arachidonic acid by cyclooxygenase (COX). COX is the rate-limiting enzyme in the conversion of arachidonic acid to PGH 2 , the substrate for the synthesis of other PGs.…”

mentioning

confidence: 99%

Correlation of Expression of Cyclooxygenase-2, Vascular Endothelial Growth Factor, and Peroxisome Proliferator–Activated Receptor δ With Head and Neck Squamous Cell Carcinoma

Jaeckel¹,

Raja²,

Tan³

et al. 2001

Arch Otolaryngol Head Neck Surg

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Cyclooxygenase (COX) is the rate-limiting enzyme in the formation of prostaglandins from arachidonic acid. COX exists in 2 isoforms, COX-1 and COX-2. These isoforms are encoded by separate genes and demonstrate cell-specific expression and regulation. Peroxisome proliferator-activated receptor delta (PPARdelta) is a nuclear transcription factor that is activated by prostacyclin. Vascular endothelial growth factor (VEGF) is a proangiogenic factor that is up-regulated in various tumors. Vascular endothelial growth factor has been shown to interact with COX-derived prostaglandins in angiogenesis. To better understand the roles of these genes in head and neck squamous cell carcinoma (HNSCCA), we examined the differential expression of the COX1, COX2, VEGF, and PPARdelta genes in these tumors. Tissue samples from patients with HNSCCA were analyzed for COX-1, COX-2, VEGF, and PPARdelta messenger RNAs (mRNAs) by in situ hybridization. COX-1 and COX-2 mRNAs were also evaluated with Northern blot hybridization. Immunohistochemistry was used to analyze for COX-2 and PPARdelta proteins. Results showed focal areas of accumulation for COX-2, VEGF, and PPARdelta but not COX-1 in human HNSCCA. Northern blot hybridization showed higher levels of COX-2 mRNA in HNSCCA than in normal tissue. This suggests a supportive role of COX-2 in development and/or progression of HNSCCA. In addition, PPARdelta may be a receptor for COX-2-produced prostaglandins in HNSCCA. There is a potential role for selective COX-2 inhibitors in the treatment of these lesions.

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“…However, the levels of prostaglandins in patients compared with healthy controls were three-and twofold higher pre-and postoperatively, respectively. 61 Thromboxane A 2 and prostacyclin, two other cyclooxygenase products, were analyzed in an additional study. Thromboxane serum levels were increased as much as 30-fold in head and neck cancer patients compared with healthy controls.…”

Section: Eicosanoid Production In Head and Neck Patientsmentioning

confidence: 99%

Arachidonic acid metabolism: A primer for head and neck surgeons

Ondrey

1998

Head & Neck

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Larynx cancer and prostaglandins

Cited by 3 publications

References 35 publications

Inhibition of Head and Neck Tumor Cell Growth With Arachidonic Acid Metabolism Inhibition

Inhibition of Head and Neck Tumor Cell Growth With Arachidonic Acid Metabolism Inhibition

Correlation of Expression of Cyclooxygenase-2, Vascular Endothelial Growth Factor, and Peroxisome Proliferator–Activated Receptor δ With Head and Neck Squamous Cell Carcinoma

Arachidonic acid metabolism: A primer for head and neck surgeons

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