Expression of p16, nm23‐H1, E‐cadherin, and CD44 Gene Products and Their Significance in Nasopharyngeal Carcinoma

Huang, Guangwu; Mo, Wuning; Kuang, Guoqian; Nong, Huitu; Wei, Meng; Sunagawa, Makoto; Kosugi, Tadayoshi

doi:10.1097/00005537-200108000-00025

Cited by 32 publications

(26 citation statements)

References 38 publications

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“…We found over-expression of cyclin D1 in 26% and the lack of expression of p16 in 96% of recurrent NPC specimens. While the level of over-expression of cyclin D1 (26%) in recurrent NPC specimens was similar to the levels of over-expression (30% [7] to 66% [9]) found in primary untreated NPC, the lack of expression of p16 in recurrent NPC specimens (96%) was significantly higher than those typically reported for primary untreated NPC (40% to 70%) [9][10][11][12].…”

Section: Discussionsupporting

confidence: 64%

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Cyclin D1 and P16 expression in recurrent nasopharyngeal carcinoma

Lin

Berry²,

Sun³

et al. 2003

Otolaryngology - Head and Neck Surgery

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Background: Cyclin D1 and p16 are involved in the regulation of G1 checkpoint and may play an important role in the tumorigenesis of nasopharyngeal carcinoma (NPC). Previous studies have examined the level of expression of cyclin D1 and p16 in primary untreated NPC but no such information is available for recurrent NPC. We set out in this study to examine the expression level of cyclin D1 and p16 in recurrent NPC that have failed previous treatment with radiation +/-chemotherapy.

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Section: Discussionsupporting

confidence: 64%

“…Over-expression of cyclin D1 and/or loss of p16 has been reported in several studies on NPC. These studies found an increased level of cyclin D1 expression in 30% [7] to 66% [9] and the lack of expression of p16 in 40% to 70% of previously untreated NPC specimens [9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Cyclin D1 and P16 expression in recurrent nasopharyngeal carcinoma

Lin

Berry²,

Sun³

et al. 2003

Otolaryngology - Head and Neck Surgery

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“…EBV microRNA-associated degradation also involves p53 downstream effectors TP53INP1 and MASPIN, suggesting that p53-dependent tumor suppression may be inhibited despite accumulation of wild-type p53 in NPC. 29 EBV microRNAs may also influence metastasis by targeting cell adhesion genes such as E-cadherin, 52 a frequently down-regulated gene in metastatic NPC. 53 Although we were unable to derive both RNA and protein from our NPC cases because of small biopsy samples, previous studies demonstrated only modestly inhibited protein production, rarely finding >4-fold reduction in protein levels.…”

Section: Discussionmentioning

confidence: 99%

Profiling of Epstein‐Barr virus‐encoded microRNAs in nasopharyngeal carcinoma reveals potential biomarkers and oncomirs

Wong

Kong

Tsang

et al. 2011

Cancer

142

133

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BACKGROUND: Epstein-Barr virus (EBV) microRNAs are abundant in nasopharyngeal carcinoma (NPC) tumors. With recent advances in serum microRNA detection, the distinct presence of EBV microRNAs in serum could aid in screening endemic regions for NPC. A proposed network of genes targeted by these microRNAs could also shed light on EBV-associated tumorigenesis. METHODS: MicroRNA microarray profiling of 5 paired NPC biopsies was followed by validation of 12 up-regulated EBV microRNAs (BART1-3p, 2-5p, 5, 6-5p, 6-3p, 7, 8, 9, 14, 17-5p, 18-5p, 19-3p) in 15 additional cases by real-time polymerase chain reaction. Tumor (cellular) and serum microRNA copy numbers from the same 15 patients were correlated. Expression of the same microRNAs were also examined in EBV-positive cell lines C666 and NP460hTERTþEBV. Bioinformatic tools helped predict cellular target genes, which were later confirmed by gene expression analysis. RESULTS: The authors' high-throughput approach shows that EBV microRNAs are generally more up-regulated than microRNAs of human origin. Twenty-nine of 39 EBV microRNAs were significantly up-regulated in tumor versus their nontumor biopsies (P < .05). Upon successfully validating 12 selected EBV microRNAs in 15 additional paired NPC cases, the authors found that their distinct presence in the serum of NPC patients positively correlated with cellular copy numbers of EBV microRNAs. Further investigation of potential EBV microRNA target genes revealed inhibition of tumor suppressor genes (eg, PTEN) and extensive deregulation of several pathways frequently involved in NPC (eg, Wnt signaling). CONCLUSIONS: Increasing knowledge of host-virus interaction via microRNAs may provide feasible explanations underlying NPC tumorigenesis along with the development of biomarkers for screening high-risk populations. Cancer 2012;118:698-

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“…Nevertheless, these etiological factors may induce aberrant expression of cell adhesion molecules (CAMs) in NPC, since CAMs govern the social behaviors of cells and altered expression of CAMs affects the motility and invasiveness of many tumor cells in vitro and metastasis in vivo (Cavallaro et al, 2004). For examples, up-regulation of ICAM (Yu et al, 2004) and down-regulation of E-cadherin (Huang et al, 2001;Li et al, 2004) and connexin 43 (Yi et al, 2006) correlates with the progression of NPC; however, the expression of CD44 does not (Huang et al, 2001). …”

mentioning

confidence: 99%

Significance of Expression of Human METCAM/MUC18 in Nasopharyngeal Carcinomas and Metastatic Lesions

Lin

Chiang²,

Wang³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Expression of p16, nm23‐H1, E‐cadherin, and CD44 Gene Products and Their Significance in Nasopharyngeal Carcinoma

Abstract: Detecting the expressions of those gene products may provide clinically valuable information for therapeutic strategy and for predicting the prognosis of patients with NPC.

Cited by 32 publications

References 38 publications

Cyclin D1 and P16 expression in recurrent nasopharyngeal carcinoma

Cyclin D1 and P16 expression in recurrent nasopharyngeal carcinoma

Profiling of Epstein‐Barr virus‐encoded microRNAs in nasopharyngeal carcinoma reveals potential biomarkers and oncomirs

Significance of Expression of Human METCAM/MUC18 in Nasopharyngeal Carcinomas and Metastatic Lesions

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