Inhibition of Cyclooxygenase‐2 Expression: An Approach to Preventing Head and Neck Cancer

Mestre, Juan R.; Chan, Georgette; Zhang, Fan; Yang, Eun Kyung; Sacks, Peter G.; Boyle, Jay O.; Shah, Jatin P.; Edelstein, David R.; Subbaramaiah, Kotha; Dannenberg, Andrew J.

doi:10.1111/j.1749-6632.1999.tb08724.x

Cited by 89 publications

(61 citation statements)

References 23 publications

(34 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…72 Indeed, our group has demonstrated that COX-2 is upregulated in oral carcinogenesis, in keeping with findings from others. 60,73 Thus, COX-2 was not expressed in normal oral mucosa, to some extent in dysplastic oral mucosa and in most specimens of oral carcinoma. Also, COX-2 was exclusively upregulated in oral premalignant lesions that were DNA aneuploid.…”

Section: Chemopreventive Strategy In Oral Premalignanciesmentioning

confidence: 96%

Retracted: Impact of genomic instability in risk assessment and chemoprevention of oral premalignancies

Reith¹,

Sudbø²

2002

Intl Journal of Cancer

View full text Add to dashboard Cite

Head-and-neck cancer is a disfiguring disease with increasing incidence rates even in young people, whose exposure to known risk factors is limited. This emphasizes the importance of early identification, on an individual basis, of precursor lesions that will develop into carcinomas. The clinical value of identifying individuals at high risk of oral cancer is emphasized by the fact that these patients are likely to benefit from available chemopreventive measures, largely without adverse effects. © 2002 Wiley-Liss, Inc. Key words : premalignant oral lesion; cancer risk; early diagnosis; prognosis; DNA ploidy; gross genomic aberration; chemoprevention; Oral squamous cell carcinomas have high mortality and morbidity and afflict an estimated 500,000 patients annually worldwide. [1][2][3][4] The incidence of oral carcinomas is especially high and increasing in developing countries. However, it is also increasing in Western countries, 5 substantially among younger people. 6 -8 Most cancers of the oral cavity are preceded by readily detectable white or red patches in the mucosal lining. The simple and straightforward detection of putative premalignant lesions gives a unique opportunity for identification of a malignant process and curative intervention at an early stage of oral carcinogenesis. Despite important advances in the field of head-and-neck oncology over the last decade, 9,10 identifying the subset of oral lesions that will progress to oral squamous cell carcinomas has remained a challenge. Reliable identification of lesions that are destined to become invasive cancers is possible. 11,12 Progress in determining the malignant potential of oral lesions allows more efficient chemopreventive treatment. 13 This review focuses on some diagnostic possibilities in premalignancies of the head and neck and on aspects of their molecular biology that may influence therapeutic approaches.PREMALIGNANT LESIONS OF THE ORAL MUCOSA Leukoplakias are frequently encountered lesions with a documented potential for transformation into oral squamous cell carcinomas. 14 -17 Erythroplakias, which are far rarer than leukoplakias, are considered to have a higher rate of malignant transformation (in some reports as high as 90%). 15 Detection of red or white patches does not require very sophisticated equipment or a particularly high degree of compliance from the patient. Since the days of Virchow, considerable knowledge of the morphologic manifestations of malignant genotypic changes has accumulated. In lesions of the oral cavity, the histologic finding of dysplasia has been considered to signal increased risk of malignant transformation. However, there is considerable uncertainty in the classification and grading of oral dysplasia, 18 -20 and several studies suggest that early and significant genetic changes do not necessarily correlate with observable morphologic changes within the mucosa. 11,12 Such changes have been detected and shown to signal subsequent transformation into manifest carcinoma, even in lesions classified as bei...

show abstract

Section: Chemopreventive Strategy In Oral Premalignanciesmentioning

confidence: 96%

Retracted: Impact of genomic instability in risk assessment and chemoprevention of oral premalignancies

Reith¹,

Sudbø²

2002

Intl Journal of Cancer

View full text Add to dashboard Cite

show abstract

“…Activation of EGFR has been shown to induce increased COX-2 expression in various normal and tumor cell lines, including HNSCC cell lines (46)(47)(48)(49)(50)(51)(52)(53)(54). Both transforming growth factor-a and epidermal growth factor, ligands of EGFR, were found to induce COX-2 expression (46 -50).…”

Section: Chemoprevention For Hncmentioning

confidence: 99%

Interaction between epidermal growth factor receptor– and cyclooxygenase 2–mediated pathways and its implications for the chemoprevention of head and neck cancer

Choe

Zhang

Shin

et al. 2005

Molecular Cancer Therapeutics

View full text Add to dashboard Cite

Head and neck squamous cell carcinoma is a well-known model for chemoprevention studies because of its field cancerization effect, its multistep carcinogenesis process, and the easy accessibility of biopsies to target lesions. With new understandings of head and neck carcinogenesis and the development of molecular targeted therapy, chemoprevention trials for head and neck squamous cell carcinoma have been rapidly updated. Cyclooxygenase-2 (COX-2) and epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors are gaining significant attention as potential chemopreventive agents. Both COX-2 and EGFR are involved in head and neck carcinogenesis. Targeting COX-2 and EGFR separately has shown promising antitumor activity. Recently, combinations of COX-2 and EGFR tyrosine kinase inhibitors have been reported to show synergistic/ additive effects in preclinical studies. Because COX-2 and EGFR tyrosine kinase inhibitors are toxic as single agents in clinical trials, the combination of COX-2 and EGFR tyrosine kinase inhibitors used at lower doses seems more promising than monotherapy with either as a novel strategy in head and neck cancer chemoprevention. [Mol Cancer Ther 2005;4(9):1448 -55]

show abstract

“…COX-2 is also overexpressed in transformed cells and in tumors (Dannenberg et al, 2001). Although chemopreventive strategies have focused on inhibitors of COX enzyme activity, the mechanism of COX-2 inhibition with anticancer activity is still well understood (Mestre et al, 1999). Moreover, selective COX-2 inhibitors have been found to prevent the formation of intestinal and skin tumors in experimental animals (Pentland et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Methyl-β-cyclodextrin inhibits cell growth and cell cycle arrest via a prostaglandin E(2) independent pathway

Choi

Chin²,

Rhee³

et al. 2004

Exp Mol Med

View full text Add to dashboard Cite

A bstractMethyl-β-cyclodextrin, a cyclic oligosaccharide know n for its interaction w ith the plasm a m em brane induces several events in cells including cell growth and anti-tum or activity. In this study, w e have investigated the possible role of cyclooxygenase 2 (COX-2) in cell growth arrest induced by m ethyl-β-cyclodextrin in Raw264.7 macrophage cells. M ethyl-β-cyclodextrin inhibited cell grow th and arrested the cell cycle, and this cell cycle arrest reduced the population of cells in the S phase, and concom itantly reduced cyclin A and D expressions. M ethyl-β-cyclodextrin in a dose-and tim e-dependent manner, also induced COX-2 expression, prostaglandin E 2 (PG E 2 ) synthesis, and CO X-2 prom oter activity. Pretreatm ent of cells w ith NS398, a CO X-2 specific inhibitor com pletely blocked PG E 2 synthesis induced by m ethyl-β-cyclodextrin, how ever inhibition on cell proliferation and cell cycle arrest w as not effected, suggesting nonas so cia tio n o f C O X -2 in th e ce ll cy cle arres t. These results suggest that m ethyl-β-cyclodextrin induced cell growth inhibition and cell cycle arrest in Raw 264.7 cells m ay be m ediated by cyclin A and D1 expression.

show abstract

Inhibition of Cyclooxygenase‐2 Expression: An Approach to Preventing Head and Neck Cancer

Cited by 89 publications

References 23 publications

Retracted: Impact of genomic instability in risk assessment and chemoprevention of oral premalignancies

Retracted: Impact of genomic instability in risk assessment and chemoprevention of oral premalignancies

Interaction between epidermal growth factor receptor– and cyclooxygenase 2–mediated pathways and its implications for the chemoprevention of head and neck cancer

Methyl-β-cyclodextrin inhibits cell growth and cell cycle arrest via a prostaglandin E(2) independent pathway

Contact Info

Product

Resources

About