The Detection of the<i>c-myc</i>and<i>ras</i>Oncogenes in Nasopharyngeal Carcinoma by Immunohistochemistry

Porter, M. J.; Field, John K.; Leung, Sing Fai; Lo, Dennis; Lee, Joseph C. K.; Spandidos, Demetrios Α.; Hasselt, C. Andrew van

doi:10.3109/00016489409126025

Cited by 51 publications

(23 citation statements)

References 14 publications

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“…Although no association has been found between the c-myc amplification and sex, gender, tumor size, clinical stage or differentiation, these investigators observed that patients with tumors with high levels of c-myc showed shortened overall survival. In addition, Porter et al (16) demonstrated c-myc amplification in 22% of tumors from the nasopharynx and observed that the prognosis for patients with tumors with c-myc amplification was worse compared with patients with tumors without c-myc amplification.…”

Section: Genetic Alterations Oncogene Activationmentioning

confidence: 99%

Genetic alterations in head and neck squamous cell carcinomas

Nagai

1999

Braz J Med Biol Res

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The genetic alterations observed in head and neck cancer are mainly due to oncogene activation (gain of function mutations) and tumor suppressor gene inactivation (loss of function mutations), leading to deregulation of cell proliferation and death. These genetic alterations include gene amplification and overexpression of oncogenes such as myc, erbB-2, EGFR and cyclinD1 and mutations, deletions and hypermethylation leading to p16 and TP53 tumor suppressor gene inactivation. In addition, loss of heterozygosity in several chromosomal regions is frequently observed, suggesting that other tumor suppressor genes not yet identified could be involved in the tumorigenic process of head and neck cancers. The exact temporal sequence of the genetic alterations during head and neck squamous cell carcinoma (HNSCC) development and progression has not yet been defined and their diagnostic or prognostic significance is controversial. Advances in the understanding of the molecular basis of head and neck cancer should help in the identification of new markers that could be used for the diagnosis, prognosis and treatment of the disease.

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Section: Genetic Alterations Oncogene Activationmentioning

confidence: 99%

Genetic alterations in head and neck squamous cell carcinomas

Nagai

1999

Braz J Med Biol Res

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“…Table I. Results of LOH analyses in two set of squamous cell carcinoma of larynx, one presented with (cases [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17] and the other without (cases 17-34) a deletion 13q21-q34 observed in CGH. …”

Section: Methodsmentioning

confidence: 99%

“…MYC, RAS, ERBB2, BCL2, and tumor suppressor genes (TSG), e.g. TP53, RB (9)(10)(11)(12)(13). A sequence of frequent allelic loss observed at 9p, 3p, 17q, 4q, 13q followed by LOH at 18q and 8p has been suggested as a critical pathway for HNSCC development and progression (14).…”

Section: Introductionmentioning

confidence: 99%

Three distinct regions of deletion on 13q in squamous cell carcinoma of the larynx

Stembalska

Blin²,

Ramsey³

et al. 2006

Oncol Rep

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Abstract. Genetic etiology of squamous cell carcinoma of the larynx (SCCL) is very complex, with both molecular and chromosomal alterations involved. The target genes have not yet been clearly identified. Therefore, our study focused on searching for regions that potentially harbor genes related to SCCL. After comparative genomic hybridization (CGH) analysis of a set of 52 SCCL we specified 13q21-q32 and 13q34 as the most frequently deleted regions. In order to precisely map the critical region of deletion, we studied these areas by using 15 microsatellite markers. In our material a significantly high frequency of loss of heterozygosity (LOH)

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“…Epstein-Barr virus (EBV), genetic factors (human HLA type A2-BW42 and cytochrome p4502E1-CYP2E1), and certain dietary (nitrosamine, herbal medicine) and environmental conditions (smoking, occupational exposures) have been shown to be involved in the development of NPC (Hildesheim and Levine, 1993), but the molecular mechanisms by which NPC was generated remained largely unknown. Overexpression of Myc oncogene was detected in NPC cell lines (Lin et al, 1993) and in some NPC tumours (Porter et al, 1994). Bcl-2 was up-regulated and was detected in most samples of NPC (Lu et al, 1993).…”

mentioning

confidence: 99%

“…Overexpression of Myc oncogene was detected in NPC cell lines (Lin et al, 1993) and in some NPC tumours (Porter et al, 1994). Bcl-2 was up-regulated and was detected in most samples of NPC (Lu et al, 1993).…”

mentioning

confidence: 99%

Elevated expression of thyroid hormone receptor α 2 (c-erb A-α2) in nasopharyngeal carcinoma*

et al. 2000

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Nasopharyngeal carcinoma (NPC) is an endemic cancer with a very high incidence in South China and Southeast Asia such as Hong-Kong and Taiwan. Epstein-Barr virus (EBV), genetic factors (human HLA type A2-BW42 and cytochrome p4502E1-CYP2E1), and certain dietary (nitrosamine, herbal medicine) and environmental conditions (smoking, occupational exposures) have been shown to be involved in the development of NPC (Hildesheim and Levine, 1993), but the molecular mechanisms by which NPC was generated remained largely unknown. Overexpression of Myc oncogene was detected in NPC cell lines (Lin et al, 1993) and in some NPC tumours (Porter et al, 1994). Bcl-2 was up-regulated and was detected in most samples of NPC (Lu et al, 1993). Mutations in p53 tumour suppressor gene (Spruck et al, 1992) and RB/p105 gene (Sun et al, 1993) in NPC are relatively rare. Lately, mutations in the RB2/p130 gene were detected in 30% of primary human NPCs (Claudio et al, 2000). Though decreased level of expression was reported, no point mutation of the potential tumour suppressor gene p16 was detected in NPC (Sun et al, 1995). These studies suggested the importance of other genes in NPC oncogenesis.Various tools such as cytogenetic analysis (Mitelman et al, 1983;Huang et al, 1989), loss of heterozygosity (LOH) (Huang et al, 1991;Hu et al, 1996;Mutirangura et al, 1997), and comparative genomic hybridization (CGH) Hui et al, 1999) have been employed to investigate the candidate genes associated with NPC. These studies offered a genome-wide investigation based upon a comprehensive pattern of DNA sequence copy number changes. Alterations due to mutations and/or regulation dysfunction can hardly be detected. Differential display (DD) (Fung et al, 1998) and cDNA representational difference analysis (RDA) (Zhan et al, 1998) offered alternative screening tools. We had adopted differential display for the study of differences in gene-expression patterns between normal nasal epithelial and transformed nasopharyngeal epithelial cells. The elevated expression of TR-α2 in NPC cell lines was demonstrated. RNA in situ hybridization of TR-α2 transcripts among biopsies derived from NPC cases and control subjects was employed to substantiate the in vitro finding. MATERIALS AND METHODS Cell cultureBiopsied tissues of nasal polyps and turbinates were collected from National Taiwan University Hospital and Mackay Memorial Hospital, Taipei. After removal of blood clots with three washes of sterile phosphate buffered saline (PBS), these samples were added into Dulbecco's minimum essential medium (DMEM) supplemented with 0.1 mM nonessential amino acids, 50 U ml -1 penicillin, 50 µg ml -1 streptomycin, 1.25 µg ml -1 fungizone and 1 mg ml -1 pronase. After an overnight incubation at 4˚C, carcass was discarded and the suspension was centrifuged at 1,500 rpm for 10 min at room temperature. The pelleted cells were resuspended in DMEM supplemented with 10% fetal bovine serum, 0.1 mM nonessential amino acids, 50 U ml -1 penicillin, 50 µg ml -1 streptomycin, 1.25 µg ml -1 fu...

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The Detection of thec-mycandrasOncogenes in Nasopharyngeal Carcinoma by Immunohistochemistry

Cited by 51 publications

References 14 publications

Genetic alterations in head and neck squamous cell carcinomas

Genetic alterations in head and neck squamous cell carcinomas

Three distinct regions of deletion on 13q in squamous cell carcinoma of the larynx

Elevated expression of thyroid hormone receptor α 2 (c-erb A-α2) in nasopharyngeal carcinoma*

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