Nasopharyngeal carcinomas

Spano, Jean Philippe; Busson, P.; Atlan, D; Bourhis, Jean; Pignon, Jean-Pierre; Esteban, Carmen; Armand, Jean‐Pierre

doi:10.1016/s0959-8049(03)00367-8

Cited by 188 publications

(164 citation statements)

References 116 publications

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“…Over 50%-70% of NPC patients present with advanced disease (stages II b-IV) with lymph node invasion or metastasis at the time of diagnosis. The rate of distant metastasis in recurrent NPC patients is up to 37% (Chan et al, 2002;Hong et al, 2010;Isobe et al, 1998;Skinner et al, 1991;Spano et al, 2003). Because of the special location of NPC, radiotherapy Fig.…”

Section: Discussionmentioning

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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Section: Discussionmentioning

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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“…The progressive declines in more recent generations could be explained by the gradual reduction of population exposures to environmental risk factors. The association of keratinising tumours with Epstein -Barr virus (EBV) has long been controversial (Spano et al, 2003), but a relationship with tobacco smoking has been found in several studies (Vaughan et al, 1996;Spano et al, 2003;Sun et al, 2005). The overall smoking prevalence which has steadily decreased in Hong Kong since the mid-1970s for both genders among Hong Kong Chinese (Tobacco Control Office, 2006) could well explain the declining trend of keratinising tumours, allowing for a 10-year lag after exposure to cigarette smoking.…”

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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“…In addition, EBV also is present in premalignant lesions, and is believed to be important for the oncogenic process in NPC. [10][11][12][13][14][15][16][17][18][19] One strategy is to treat these tumors as immune targets and directly manipulate preexisting virusspecific cytotoxic T-lymphocytes (CTLs) to attack epitopes derived from viral proteins and presented by infected tumor cells. Prior studies have established the feasibility and safety of EBV-stimulated cytotoxic T-lymphocyte (EBV-CTL) immunotherapy in a variety of EBV-related neoplasms and proliferations, suggesting potential efficacy against NPC.…”

Section: Introductionmentioning

confidence: 99%

Epstein‐Barr virus‐specific adoptive immunotherapy for recurrent, metastatic nasopharyngeal carcinoma

Huang

Fogg

Wirth

et al. 2017

Cancer

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BACKGROUND: Early-stage and intermediate-stage nasopharyngeal cancer (NPC) generally carry a good prognosis, but for patients with recurrent, metastatic disease, options are limited. In the current study, the authors present a phase 1/2 study to evaluate the efficacy of Epstein-Barr virus (EBV)-stimulated cytotoxic T-lymphocyte (EBV-CTL) immunotherapy in this patient population. METHODS: Screening for patients with active, recurrent, metastatic EBV-associated NPC began in February 2007, and the study was closed to accrual in January 2012. After informed consent was obtained, patients had their blood drawn to initiate manufacturing of the EBV-CTL product. During product manufacturing, patients were placed on interim standard-of-care chemotherapy, and only after disease progression on the interim chemotherapy did patients receive investigational immunotherapy. Patients were restaged every 2 months until disease progression and then followed for survival. RESULTS: A total of 28 patients were enrolled, and 21 patients were treated. There was 1 complete response achieved, and at the time of last follow-up, the patient had been in remission for >8 years since treatment. The median progression-free survival was 2.2 months, and the median overall survival was 16.7 months. Two other patients, after failing EBV-CTL immunotherapy, unexpectedly demonstrated strong responses to the chemotherapy regimens they had previously failed. Patient EBV viral load and EBV-CTL specificity for tumor-associated viral antigens did not appear to correlate with clinical response. CONCLUSIONS: A durable response was observed with EBV-CTL immunotherapy, but the overall response rate for patients with recurrent, metastatic NPC was low. Further research is necessary to increase the efficacy of EBV-specific immunotherapy in patients with incurable NPC, and to characterize mechanisms for refacilitation to chemotherapy.

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Nasopharyngeal carcinomas

Cited by 188 publications

References 116 publications

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

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

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

Epstein‐Barr virus‐specific adoptive immunotherapy for recurrent, metastatic nasopharyngeal carcinoma

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