Nasopharyngeal carcinoma causes: Difference between revisions
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==Overview== | ==Overview== | ||
Common [[causes]] of nasopharyngeal carcinoma include [[Epstein Barr virus]] ([[EBV infection|EBV infection)]], [[Human papillomavirus|Human Papillomavirus]] ([[HPV infection]]), and consumption of salted fish as a source of N-nitrosamine. | |||
==Causes== | |||
===Common Causes=== | |||
Common [[causes]] of nasopharyngeal carcinoma may include: | |||
*[[EBV infection]] : EBV infection | |||
*[[HPV infection]] | |||
*Consumption of salted fish as a source of N-nitrosamine | |||
EBV infection is perhaps the most extensively studied | |||
aetiological factor for nasopharyngeal carcinoma. On the | |||
basis of in-situ hybridisation techniques to EBV-encoded | |||
RNAs, the virus is detected exclusively in all tumour cells | |||
but not in normal nasopharyngeal epithelium, suggesting | |||
that EBV activation is necessary in the pathogenesis of | |||
nasopharyngeal carcinoma. This notion is further | |||
supported by reports that similar techniques undertaken | |||
on preinvasive lesions identifi ed the presence of EBV even | |||
during the initial phases of malignant transformation.6,7 | |||
Yet, the inability to detect EBV in nasopharyngeal biopsy | |||
samples from high-risk individuals suggests that other | |||
factors are needed for the EBV-infected epithelial cell to | |||
undergo malignant transformation. Recent work has | |||
proposed that deregulation of cell-cycle checkpoint | |||
through p16 inactivation and cyclin D1 overexpression | |||
promotes maintenance of the viral genome, favouring | |||
transition of low-grade dysplasia to higher grade lesions.8,9 | |||
Intrinsic genetic determinants such as 3p and 9p deletions | |||
have also been suggested as mechanisms of susceptibility | |||
to EBV infection and its downstream eff ects.10 Epigenetic | |||
modifi cations that are associated with a tumorigenic | |||
phenotype have been identifi ed in EBV-infected epithelial | |||
cells and were shown to persist even in the absence of the | |||
virus (appendix). | |||
[[Category: (name of the system)]] | [[Category: (name of the system)]] | ||
Revision as of 15:33, 5 March 2019
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Homa Najafi, M.D.[2]Faizan Sheraz, M.D. [3]
Overview
Common causes of nasopharyngeal carcinoma include Epstein Barr virus (EBV infection), Human Papillomavirus (HPV infection), and consumption of salted fish as a source of N-nitrosamine.
Causes
Common Causes
Common causes of nasopharyngeal carcinoma may include:
- EBV infection : EBV infection
- HPV infection
- Consumption of salted fish as a source of N-nitrosamine
EBV infection is perhaps the most extensively studied
aetiological factor for nasopharyngeal carcinoma. On the
basis of in-situ hybridisation techniques to EBV-encoded
RNAs, the virus is detected exclusively in all tumour cells
but not in normal nasopharyngeal epithelium, suggesting
that EBV activation is necessary in the pathogenesis of
nasopharyngeal carcinoma. This notion is further
supported by reports that similar techniques undertaken
on preinvasive lesions identifi ed the presence of EBV even
during the initial phases of malignant transformation.6,7
Yet, the inability to detect EBV in nasopharyngeal biopsy
samples from high-risk individuals suggests that other
factors are needed for the EBV-infected epithelial cell to
undergo malignant transformation. Recent work has
proposed that deregulation of cell-cycle checkpoint
through p16 inactivation and cyclin D1 overexpression
promotes maintenance of the viral genome, favouring
transition of low-grade dysplasia to higher grade lesions.8,9
Intrinsic genetic determinants such as 3p and 9p deletions
have also been suggested as mechanisms of susceptibility
to EBV infection and its downstream eff ects.10 Epigenetic
modifi cations that are associated with a tumorigenic
phenotype have been identifi ed in EBV-infected epithelial
cells and were shown to persist even in the absence of the
virus (appendix).