Update from the 5th Edition of the World Health Organization Classification of Head and Neck Tumors: Oropharynx and Nasopharynx

Badoual, Cécile

doi:10.1007/s12105-022-01449-2

Cited by 40 publications

(28 citation statements)

References 79 publications

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“…NPC is the closest EBV-associated endemic disease, in which has higher prevalence in Africa and Southeast Asia, but lower incidence in western countries. According to the latest tumor classification by the World Health Organization (WHO) (5 th edition), NPC can be divided into three categories: keratinizing squamous cell carcinoma (type I), non-keratinizing squamous cell carcinoma (type II), and basaloid squamous cell carcinoma (type III) (Badoual, 2022). Non-keratinizing NPC is predominantly associated with EBV infection, of which nearly 100% of the undifferentiated and partially differentiated cases are detected as EBV-positive (Young and Dawson, 2014).…”

Section: Ebv Infection In Tumorigenesismentioning

confidence: 99%

EBV Infection and Its Regulated Metabolic Reprogramming in Nasopharyngeal Tumorigenesis

Yang

You

Meng³

et al. 2022

Front. Cell. Infect. Microbiol.

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Viral oncogenes may drive cellular metabolic reprogramming to modulate the normal epithelia cell malignant transformation. Understanding the viral oncogene–mediated signaling transduction dysregulation that involves in metabolic reprogramming may provide new therapeutic targets for virus-associated cancer treatment. Latent EBV infection and expression of viral oncogenes, including latent membrane proteins 1 and 2 (LMP1/2), and EBV-encoded BamH I-A rightward transcripts (BART) microRNAs (miR-BARTs), have been demonstrated to play fundamental roles in altering host cell metabolism to support nasopharyngeal carcinoma (NPC) pathogenesis. Yet, how do EBV infection and its encoded oncogenes facilitated the metabolic shifting and their roles in NPC carcinogenesis remains unclear. In this review, we will focus on delineating how EBV infection and its encoded oncoproteins altered the metabolic reprograming of infected cells to support their malignances. Furthermore, based on the understanding of the host’s metabolic signaling alterations induced by EBV, we will provide a new perspective on the interplay between EBV infection and these metabolic pathways and offering a potential therapeutic intervention strategy in the treatment of EBV-associated malignant diseases.

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Section: Ebv Infection In Tumorigenesismentioning

confidence: 99%

EBV Infection and Its Regulated Metabolic Reprogramming in Nasopharyngeal Tumorigenesis

Yang

You

Meng³

et al. 2022

Front. Cell. Infect. Microbiol.

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“…Nasopharyngeal carcinoma (NPC) is a head-and-neck squamous-cell carcinoma (HNSCC) that originates in the nasopharyngeal epithelium [ 1 ]. According to the World Health Organization (WHO) histopathological classification, NPC is classified as keratinizing squamous-cell carcinoma, non-keratinizing carcinoma, and basaloid squamous-cell carcinoma [ 2 ]. In addition, non-keratinizing nasopharyngeal carcinoma is subdivided into differentiated non-keratinizing carcinoma (WHO classification, type II) and undifferentiated non-keratinizing carcinoma (WHO classification, type III) [ 2 , 3 ].…”

Section: Introductionmentioning

confidence: 99%

“…According to the World Health Organization (WHO) histopathological classification, NPC is classified as keratinizing squamous-cell carcinoma, non-keratinizing carcinoma, and basaloid squamous-cell carcinoma [ 2 ]. In addition, non-keratinizing nasopharyngeal carcinoma is subdivided into differentiated non-keratinizing carcinoma (WHO classification, type II) and undifferentiated non-keratinizing carcinoma (WHO classification, type III) [ 2 , 3 ]. NPC has a high incidence in southern China and some Southeast Asian regions, yet is extremely rare in most parts of the world [ 1 ].…”

Section: Introductionmentioning

confidence: 99%

Nasopharyngeal Carcinoma Progression: Accumulating Genomic Instability and Persistent Epstein–Barr Virus Infection

Deng

Huang

et al. 2022

Current Oncology

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Genomic instability facilitates the evolution of cells, tissues, organs, and species. The progression of human malignancies can be regarded as the accumulation of genomic instability, which confers a high evolutionary potential for tumor cells to adapt to continuous changes in the tumor microenvironment. Nasopharyngeal carcinoma (NPC) is a head-and-neck squamous-cell carcinoma closely associated with Epstein–Barr virus (EBV) infection. NPC progression is driven by a combination of accumulated genomic instability and persistent EBV infection. Here, we present a review of the key characteristics of genomic instability in NPC and the profound implications of EBV infection. We further discuss the significance of profiling genomic instability for the assessment of disease progression and treatment efficacy, as well as the opportunities and challenges of targeted therapies for NPC based on its unique genomic instability.

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“…Although NPC is a kind of HNSCC, it shows evident differences from other HNSCCs. For example, most tissues of NPC have unique characteristics of undifferentiated nonkeratinizing in endemic regions (Badoual, 2022). According to the National Comprehensive Cancer Network guidelines, NPC definitely differs from HNSCC.…”

Section: Introductionmentioning

confidence: 99%

ZBTB7A governs 2-DG-inhibited glycolysis by regulating GLUT1 in nasopharyngeal carcinoma

LIU¹,

Wei²,

Lan³

et al. 2022

Biocell

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Our previous studies suggested a potential interaction between the POK erythroid myeloid ontogenic factor ZBTB7A and glucose transporter 1 (GLUT1) in nasopharyngeal carcinoma (NPC). This study was designed to confirm the interaction and further evaluate the precise mechanism by which ZBTB7A and GLUT1 regulate NPC development. The binding sites between ZBTB7A and the promoter of GLUT1 were predicted by bioinformatics.Gene expression was measured by quantitative real-time polymerase chain reaction (qPCR), western blotting, and immunohistochemistry. The activities of key glycolysis enzymes, including hexokinase (HK), pyruvate kinase (PK), lactate dehydrogenase (LDH), and lactate, were detected using specific enzyme-linked immunosorbent assay kits. The connection between ZBTB7A and GLUT1 was analyzed by dual-luciferase reporter assay and chromatin immunoprecipitation-qPCR. The vitality, proliferation, and tumorigenicity of the cells expressing different levels of ZBTB7A were tested by adding the glycolysis inhibitor 2-deoxy-D-glucose (2-DG), followed by MTT, colorimetric focus forming, and xenograft assays, respectively. Our results showed that high expression of GLUT1 was associated with late-stage NPC. After constructing stably transfected cells with lentiviruses, ZBTB7A was effectively knocked down in 5-8F cells (RNAi-5-8F) and overexpressed in 6-10B cells (ZBTB7A-6-10B). The up-or downregulation of GLUT1 secondary to ZBTB7A changes was also limited. The vitality and proliferation of the cells expressing low ZBTB7A were notably blocked by 2-DG. The cells expressing high ZBTB7A were not very sensitive to 2-DG. The growth of RNAi-5-8F xenografts was strongly suppressed by 2-DG. The activities of HK, PK, and LDH were suppressed by 2-DG in the cells expressing low ZBTB7A. RNAi-5-8F cells had the lowest 2-DG-induced lactate production. ZBTB7A directly suppressed the promoter region of GLUT1 to regulate GLUT1 expression. Thus, ZBTB7A controls the 2-DG-induced inhibition of glycolysis by affecting GLUT1.

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Update from the 5th Edition of the World Health Organization Classification of Head and Neck Tumors: Oropharynx and Nasopharynx

Cited by 40 publications

References 79 publications

EBV Infection and Its Regulated Metabolic Reprogramming in Nasopharyngeal Tumorigenesis

EBV Infection and Its Regulated Metabolic Reprogramming in Nasopharyngeal Tumorigenesis

Nasopharyngeal Carcinoma Progression: Accumulating Genomic Instability and Persistent Epstein–Barr Virus Infection

ZBTB7A governs 2-DG-inhibited glycolysis by regulating GLUT1 in nasopharyngeal carcinoma

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