scholarly journals Faktor-faktor penyebab terjadinya karsinoma nasofaring (KNF)

2020 ◽  
Vol 2 (1) ◽  
pp. 113-120
Author(s):  
Nur Suci Amanah

Nasopharyngeal carcinoma is a common disease in southern China. The etiologies of the main factors proposed for the pathogenesis of KNF include genetic factors, environmental factors and Epstein Barr Virus (EBV) infection. Other causes besides preserved food consumption include salted fish which have been involved in the etiology of NPC. The downward trend in the incidence of NPC has occurred in Hong Kong for the past 20 years, which is caused by changes in dietary habits. Despite the close relationship of EBV infection with NPC, the etiological role of EBV in the pathogenesis of NPC remains an interaction. EBV infection in primary nasopharyngeal epithelial cells occurs. Epstein Barr virus does not convert primary nasopharyngeal epithelial cells into proliferative clones, which is in sharp contrast to the well-documented ability of EBV to alter and perpetuate primary B cells. Genetic changes that are supported in the nasopharyngeal epithelium may be needed to support stable EBV infection. Non-viral factors as a cause of nasopharyngeal carcinoma still cannot be resolved with certainty. Non-viral factors are one of the risk factors that can increase the number of events arising from nasopharyngeal malignancies such as smoke, salted fish, formaldehyde, genetic, as soon as possible firewood, wood dust, chronic infection, throat protector, alcohol and traditional medicine.

Cancers ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2722
Author(s):  
Fenggang Yu ◽  
Yanan Lu ◽  
Yingying Li ◽  
Yuji Uchio ◽  
Utomo Andi Pangnguriseng ◽  
...  

Epstein–Barr virus (EBV) is a human oncogenic virus that causes several types of tumor, such as Burkitt’s lymphoma and nasopharyngeal carcinoma (NPC). NPC tumor cells are clonal expansions of latently EBV-infected epithelial cells. However, the mechanisms by which EBV transforms the nasopharyngeal epithelium is hampered, because of the lack of good in vitro model to pursue oncogenic process. Our primary nasopharyngeal epithelial cell cultures developed pseudostratified epithelium at the air-liquid interface, which was susceptible to EBV infection. Using the highly sensitive RNA in situ hybridization technique, we detected viral infection in diverse cell types, including ciliated cells, goblet cells, and basal cells. EBV-encoded small RNA-positive cells were more frequently detected in the suprabasal layer than in the basal layer. We established the most physiologically relevant EBV infection model of nasopharyngeal epithelial cells. This model will advance our understanding of EBV pathogenesis in the development of NPC.


1987 ◽  
Vol 90 (9) ◽  
pp. 1334-1338
Author(s):  
TORU TAKIMOTO ◽  
TAMEO MIYAZAKI ◽  
JUNICHI IWAWAKI ◽  
SHIGERU ISHIKAWA ◽  
SAICHIROH TANAKA ◽  
...  

2017 ◽  
Vol 372 (1732) ◽  
pp. 20160270 ◽  
Author(s):  
Sai Wah Tsao ◽  
Chi Man Tsang ◽  
Kwok Wai Lo

Epstein–Barr virus (EBV) is associated with multiple types of human cancer, including lymphoid and epithelial cancers. The closest association with EBV infection is seen in undifferentiated nasopharyngeal carcinoma (NPC), which is endemic in the southern Chinese population. A strong association between NPC risk and the HLA locus at chromosome 6p has been identified, indicating a link between the presentation of EBV antigens to host immune cells and NPC risk. EBV infection in NPC is clonal in origin, strongly suggesting that NPC develops from the clonal expansion of a single EBV-infected cell. In epithelial cells, the default program of EBV infection is lytic replication. However, latent infection is the predominant mode of EBV infection in NPC. The establishment of latent EBV infection in pre-invasive nasopharyngeal epithelium is believed to be an early stage of NPC pathogenesis. Recent genomic study of NPC has identified multiple somatic mutations in the upstream negative regulators of NF-κB signalling. Dysregulated NF-κB signalling may contribute to the establishment of latent EBV infection in NPC. Stable EBV infection and the expression of latent EBV genes are postulated to drive the transformation of pre-invasive nasopharyngeal epithelial cells to cancer cells through multiple pathways. This article is part of the themed issue ‘Human oncogenic viruses’.


2019 ◽  
Vol 100 (6) ◽  
pp. 999-1012 ◽  
Author(s):  
Pei Shin Pang ◽  
Tengfei Liu ◽  
Weitao Lin ◽  
Chi-Man Tsang ◽  
Yim-Ling Yip ◽  
...  

2020 ◽  
Vol 8 (1) ◽  
pp. 60-67
Author(s):  
Ngo Dong Kha ◽  
Huynh Thi Mong Tuyen ◽  
Lam Hong Ngoc ◽  
Thieu Hong Hue ◽  
Le Quang Anh Tuan ◽  
...  

Epstein-Barr virus (EBV) infection is the main cause of Nasopharyngeal Carcinoma (NPC). EBNA-2, one of the most important genes participating in the formation of NPC, also helps EBV evade an attack on the immune system. EBNA-2 has 4 variants including E2-A, E2-B, E2-C and E-2D, of which E2-A and E2-C are the characterized variants for NPC. This study aimed to evaluate the variations of EBNA-2 in NPC biopsy samples of Vietnamese patients. This initial study used 10 biopsy samples, which were positively confirmed to NPC, collected from Cho Ray Hospital. Nested PCR – nucleotide sequencing was applied to analyze the variants of EBNA-2. The results showed that 8 out of 10 samples, accounting for 80%, were positive to EBNA-2. Additionally, only two variants, E-2A and E-2C were detected in our study, in which, E2-A subtype was identified as the predominant subtype. These findings would provide initial data about potential contribution of EBNA-2 polymorphisms to etiology of NPC in Vietnamese population.


2021 ◽  
Vol 17 (8) ◽  
pp. e1009783
Author(s):  
Nicholas Van Sciver ◽  
Makoto Ohashi ◽  
Nicholas P. Pauly ◽  
Jillian A. Bristol ◽  
Scott E. Nelson ◽  
...  

The Epstein-Barr virus (EBV) human herpesvirus is associated with B-cell and epithelial-cell malignancies, and both the latent and lytic forms of viral infection contribute to the development of EBV-associated tumors. Here we show that the Hippo signaling effectors, YAP and TAZ, promote lytic EBV reactivation in epithelial cells. The transcriptional co-activators YAP/TAZ (which are inhibited by Hippo signaling) interact with DNA-binding proteins, particularly TEADs, to induce transcription. We demonstrate that depletion of either YAP or TAZ inhibits the ability of phorbol ester (TPA) treatment, cellular differentiation or the EBV BRLF1 immediate-early (IE) protein to induce lytic EBV reactivation in oral keratinocytes, and show that over-expression of constitutively active forms of YAP and TAZ reactivate lytic EBV infection in conjunction with TEAD family members. Mechanistically, we find that YAP and TAZ interact with, and activate, the EBV BZLF1 immediate-early promoter. Furthermore, we demonstrate that YAP, TAZ, and TEAD family members are expressed at much higher levels in epithelial cell lines in comparison to B-cell lines, and find that EBV infection of oral keratinocytes increases the level of activated (dephosphorylated) YAP and TAZ. Finally, we have discovered that lysophosphatidic acid (LPA), a known YAP/TAZ activator that plays an important role in inflammation, induces EBV lytic reactivation in epithelial cells through a YAP/TAZ dependent mechanism. Together these results establish that YAP/TAZ are powerful inducers of the lytic form of EBV infection and suggest that the ability of EBV to enter latency in B cells at least partially reflects the extremely low levels of YAP/TAZ and TEADs in this cell type.


Cancers ◽  
2018 ◽  
Vol 10 (7) ◽  
pp. 237 ◽  
Author(s):  
Asuka Nanbo ◽  
Harutaka Katano ◽  
Michiyo Kataoka ◽  
Shiho Hoshina ◽  
Tsuyoshi Sekizuka ◽  
...  

Infection of Epstein–Barr virus (EBV), a ubiquitous human gamma herpesvirus, is associated with various malignancies in B lymphocytes and epithelial cells. EBV encodes 49 microRNAs in two separated regions, termed the BART and BHRF1 loci. Although accumulating evidence demonstrates that EBV infection regulates the profile of microRNAs in the cells, little is known about the microRNAs in exosomes released from infected cells. Here, we characterized the expression profile of intracellular and exosomal microRNAs in EBV-negative, and two related EBV-infected Burkitt lymphoma cell lines having type I and type III latency by next-generation sequencing. We found that the biogenesis of exosomes is upregulated in type III latently infected cells compared with EBV-negative and type I latently infected cells. We also observed that viral and several specific host microRNAs were predominantly incorporated in the exosomes released from the cells in type III latency. We confirmed that multiple viral microRNAs were transferred to the epithelial cells cocultured with EBV-infected B cells. Our findings indicate that EBV infection, in particular in type III latency, modulates the biogenesis of exosomes and the profile of exosomal microRNAs, potentially contributing to phenotypic changes in cells receiving these exosomes.


Cancers ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2441 ◽  
Author(s):  
Timmy Richardo ◽  
Pongphol Prattapong ◽  
Chawalit Ngernsombat ◽  
Nurulfitri Wisetyaningsih ◽  
Hisashi Iizasa ◽  
...  

Nasopharyngeal carcinoma (NPC) is one of the most common tumors occurring in China and Southeast Asia. Etiology of NPC seems to be complex and involves many determinants, one of which is Epstein-Barr virus (EBV) infection. Although evidence demonstrates that EBV infection plays a key role in NPC carcinogenesis, the exact relationship between EBV and dysregulation of signaling pathways in NPC needs to be clarified. This review focuses on the interplay between EBV and NPC cells and the corresponding signaling pathways, which are modulated by EBV oncoproteins and non-coding RNAs. These altered signaling pathways could be critical for the initiation and progression of NPC.


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