The aetiology of nasopharyngeal carcinoma

McDermott, Aidan; Dutt, Sunil; Watkinson, John

doi:10.1046/j.1365-2273.2001.00449.x

Cited by 208 publications

(161 citation statements)

References 64 publications

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“…To date, EBV seems to be exclusively associated with undifferentiated carcinoma in the nasopharynx (McDermott et al, 2001). However, this virus is ubiquitous and exposure to it has probably remained stable through recent generations.…”

Section: Discussionmentioning

confidence: 99%

Incidence rate trends of histological subtypes of nasopharyngeal carcinoma in Hong Kong

Tse

Mang

et al. 2006

Br J Cancer

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Section: Discussionmentioning

confidence: 99%

Incidence rate trends of histological subtypes of nasopharyngeal carcinoma in Hong Kong

Tse

Mang

et al. 2006

Br J Cancer

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“…The annual incidence of NPC is 25-50 cases per 100,000 people in Southern China, which is 100-fold higher than in western countries (3). Currently, radiotherapy is the most common therapeutic strategy for NPC, although chemotherapy is used as an adjuvant to treat advanced carcinoma and to enhance the radiosensitivity (4,5).…”

Section: Introductionmentioning

confidence: 99%

Zoledronic acid reverses cisplatin resistance in nasopharyngeal carcinoma cells by activating the mitochondrial apoptotic pathway

You

Chen

et al. 2017

Oncology Letters

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Abstract. Despite improvements to radiotherapeutic strategies, resistance to adjuvant chemotherapy remains the main problem underlying the low 5-year survival rate in patients with nasopharyngeal carcinoma (NPC). In the present study, the human NPC cell line HNE1 was exposed to gradually increasing concentrations of cisplatin (CDDP) in order to establish a drug-resistant sub-cell line, HNE1/CDDP. HNE1/CDDP cells exhibited multidrug resistance and a prolonged doubling time, as compared with the parent HNE1 cells. Furthermore, pretreatment with zoledronic acid (ZOL) appeared to resensitize the CDDP-resistant cells by inducing S-phase cell cycle arrest and the mitochondrial apoptotic pathway by upregulating the expression of B-cell lymphoma-2 (BCL-2)-associated X protein and caspase-9 and downregulating the expression of BCL-2. The results of the present study suggested that HNE1/CDDP cells are a stable, multidrug-resistant NPC cell line that may serve as an important tool for research in drug resistance. In addition, the application of ZOL may hold clinical therapeutic potential for the treatment of drug resistance in NPC.

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“…It is endemic in southern parts of China, Southeast Asia, the Mediterranean basin, and Alaska (McDermott et al, 2001). Epidemiologic investigations suggest that the etiology of NPC is associated with a complex interaction of genetic, viral, environmental, and dietary factors (Yip et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Metformin Induces G1 Cell Cycle Arrest and Inhibits Cell Proliferation in Nasopharyngeal Carcinoma Cells

Zhao

Wen

Jia

et al. 2011

The Anatomical Record

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It has been reported that metformin, a biguanide derivative widely used in type II diabetic patients, has antitumor activities in some cancers by activation of AMP-activated protein kinase (AMPK). But its role in nasopharyngeal carcinoma (NPC) is not known. Here, we reported for the first time that 1-50 mM of metformin in a dose-and time-dependent manner suppressed cell proliferation and colony formation in NPC cell line, C666-1. Further studies revealed that the protein level of cyclin D1 decreased and the percentage of the cells in G0/G1 phase increased by 5 mM metformin treatment. Metformin also induced the phosphorylation of AMPK (T172) in a time-dependent manner. Mammalian target of rapamycin complex 1 (mTORC1), which is negatively regulated by AMPK and plays a central role in cell growth and proliferation, was inhibited by metformin, as manifested by dephosphorylation of its downstream targets 40S ribosomal S6 kinase 1 (S6K1) (T389), the eukaryotic translation initiation factor 4E (eIF4E)-binding protein 1 (4E-BP1) (T37/46) and S6 (S235/236) in C666-1 cells. In a summary, metformin prevents proliferation of C666-1 cells by down-regulating cyclin D1 level and inducing G1 cell cycle arrest. AMPK-mediated inhibition of mTORC1 signaling may be involved in this process. Anat Rec, 294:1337Rec, 294: -1343Rec, 294: , 2011. V V C 2011 Wiley-Liss, Inc.

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The aetiology of nasopharyngeal carcinoma

Cited by 208 publications

References 64 publications

Incidence rate trends of histological subtypes of nasopharyngeal carcinoma in Hong Kong

Incidence rate trends of histological subtypes of nasopharyngeal carcinoma in Hong Kong

Zoledronic acid reverses cisplatin resistance in nasopharyngeal carcinoma cells by activating the mitochondrial apoptotic pathway

Metformin Induces G1 Cell Cycle Arrest and Inhibits Cell Proliferation in Nasopharyngeal Carcinoma Cells

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