Objectives To identify whether Epstein Barr virus (EBV) encoded latent membrane protein 1 (LMP1) can induce tumor necrosis factor receptor associated factor 1 (TRAF1) expression and promote its anti apoptosis acti...Objectives To identify whether Epstein Barr virus (EBV) encoded latent membrane protein 1 (LMP1) can induce tumor necrosis factor receptor associated factor 1 (TRAF1) expression and promote its anti apoptosis activity via the NF κB signaling pathway, and assess that LMP1 suppresses apoptosis in nasopharyngeal carcinoma (NPC) Methods A stable transfected cell line HNE2 LMP1 was established by introducing LMP1 cDNA into HNE2 cells Transactivation of TRAF1 was determined by luciferase reporter assay, while expression of TRAF1 mRNA was detected by RT PCR and expression of TRAF1 protein and caspase 3 by Western blot analysis Apoptosis activity was observed through fluorescence staining Results LMP1 induced TRAF1 expression in NPC cells and caused a decrease in apoptosis This induction could be blocked by antisense LMP1 Moreover, LMP1 mediated induction of a TRAF1 promoter driven reporter gene was significantly impaired when the κB site κB1 or κB5 was disrupted, whereas mutation of κB3 had only a minor effect on LMP1 dependent up regulation of the reporter gene Conclusion LMP1 induces TRAF1 expression and promotes its anti apoptosis activity via the NF κB signaling pathway, which may be one of the mechanisms that LMP1 uses to suppress apoptosis in NPC cells展开更多
AIM:To verify the methylation status of CDH1, DAPK, COX2, hMLH1 and CDKN2A genes and to evaluate their association with Helicobacter pylori (H. pylori)-cagA+ and Epstein Barr virus (EBV) infections in gastric adenocar...AIM:To verify the methylation status of CDH1, DAPK, COX2, hMLH1 and CDKN2A genes and to evaluate their association with Helicobacter pylori (H. pylori)-cagA+ and Epstein Barr virus (EBV) infections in gastric adenocarcinomas.METHODS: Methylation-specific PCR (MSP) assay was performed in 89 primary gastric carcinomas (intestinal and diffuse types). Microsatellite instability (MSI) analysis was performed using the BAT26 primer set and PCR products were analyzed with the ABI PRISM 3100 Genetic Analyzer using Genescan 3.7 software (Applied Biosystems). Detection of H. pylori and genotyping were performed by PCR, using specifi c primers for ureaseC and cagA genes. The presence of EBV was assessed by in situ hybridization. Statistical analyses were performed using the χ2 or Fisher's exact test.RESULTS: The most frequent hypermethylated gene was COX-2 (63.5%) followed by DAPK (55.7%), CDH1 (51%), CDKN2A (36%) and hMLH1 (30.3%). Intestinal and diffuse adenocarcinomas showed different methylation profiles and there was an association between methylation of E-CDH1 and H. pylori-cagA+ in the intestinal adenocarcinoma type. MSI was correlated with hMLH1 methylation. There was an inverse correlation between DAPK hypermethylation and MSI.CONCLUSION: We found a strong association between CDH1 methylation and H. pylori-cagA+ in intestinal-type gastric cancer, association of MSI and better prognosis and an heterogeneous COX-2 overexpression.展开更多
Although many studies have found a kind of a relationship between an Epstein-Barr Virus (EBV) and the development of Multiple Sclerosis (MS), a fundamental aspect of this relationship remains uncertain. What is the ca...Although many studies have found a kind of a relationship between an Epstein-Barr Virus (EBV) and the development of Multiple Sclerosis (MS), a fundamental aspect of this relationship remains uncertain. What is the cause of Multiple Sclerosis (MS)? In this study, we re-analysed the data as published by Wandinger et al. and were able to establish a new insight: without an Epstein-Barr Virus (EBV) infection no development of Multiple Sclerosis (MS). Furthermore, we determined a highly significant causal relationship between Epstein-Barr Virus (EBV) and multiple sclerosis. Altogether, Epstein-Barr Virus (EBV) is the cause of multiple sclerosis (p-value 0.0004251570).展开更多
Objective To detect whether Epstein Barr virus (EBV) harbors in nasopharyngeal lymphoid hyperplasia (NPLH) which is frequently to be seen in Guangzhou, a high incidence area of nasopharyngeal carcinoma (NPC), ...Objective To detect whether Epstein Barr virus (EBV) harbors in nasopharyngeal lymphoid hyperplasia (NPLH) which is frequently to be seen in Guangzhou, a high incidence area of nasopharyngeal carcinoma (NPC), and to explore the relation between NPLH and development of NPC Methods Twenty four 10% formalin fixed, paraffin embedded biopsies oef patients with NPLH and elevated serum IgA antibody titer (≥1∶20) against viral capsid antigen of EB virus (IgA/VCA) were collected from the archives of the Department of Pathology, Sun Yat sen University of Medical Sciences during the period of January to June, 1993 PCR plus Southern blotting hybridization for detection of EBV DNA W fragment and in situ hybridization for detection of EB virus encoded small RNAs (EBERs) were performed All the patients were followed up more than 5 years Results Twenty two of 24 (91 7%) NPLH tissues contained EBV DNA A few definitely EBERs positive B lymphocytes could be found in 17 out of 24 specimens (70 8%) Neither NPC nor any EBV associated malignancies were developed in all of these 24 patients up to date Conclusion Most of the NPLH tissues taken from the patients with an elevated serum IgA/VCA titer carry EBV, which is harbouring in the nuclei of a few infiltrating and hyperplastic B lymphocytes The NPLH without epithelial dysplasia can not be recognized as a precancerous lesion, and EBV infection in these lesions is not an important event, having no substantial significance in development of NPC展开更多
Epstein Barr virus （EBV） positive mucocutaneous ulcers（EBVMCU） form part of a spectrum of EBV-associatedlymphoproliferative disease. They have been reportedin the setting of immunosenescence and iatrogenicimmunosu...Epstein Barr virus （EBV） positive mucocutaneous ulcers（EBVMCU） form part of a spectrum of EBV-associatedlymphoproliferative disease. They have been reportedin the setting of immunosenescence and iatrogenicimmunosuppression, affecting the oropharyngeal mucosa,skin and gastrointestinal tract （GIT）. Case reports andseries to date suggest a benign natural history respondingto conservative management, particularly in the GIT. Wereport an unusual case of EBVMCU in the colon, arisingin the setting of immunosuppression in the treatment ofCrohn＇s disease, with progression to Hodgkin lymphoma18 mo after cessation of infliximab. The patient presentedwith multiple areas of segmental colonic ulceration,histologically showing a polymorphous infiltrate withEBV positive Reed-Sternberg-like cells. A diagnosisof EBVMCU was made. The ulcers failed to regressupon cessation of infliximab and methotrexate for 18mo. Following commencement of prednisolone for herCrohn＇s disease, the patient developed widespreadHodgkin lymphoma which ultimately presented as alife-threatening lower GIT bleed requiring emergencycolectomy. This is the first report of progression ofEBVMCU to Hodgkin lymphoma, in the setting of ongoingiatrogenic immunosuppression and inflammatory boweldisease.展开更多
In a recent study published in Cell,Vietzen and colleagues discovered the novel role of natural killer(NK)cells and EBVspecific CD8+T cell response in controlling EBV-inducing autoimmune response and collectively defi...In a recent study published in Cell,Vietzen and colleagues discovered the novel role of natural killer(NK)cells and EBVspecific CD8+T cell response in controlling EBV-inducing autoimmune response and collectively defined virus and host genetics factors associated with a significantly raised risk of multiple sclerosis.展开更多
Epstein-Barr virus (EBV) encoded latent membrane protein 1 (LMP1) may trigger the transcription factor AP-1 including c-Jun and c-fos. In this report, using a Tet-on LMP1 HNE2 cell line which is a dual-stable LMP1 int...Epstein-Barr virus (EBV) encoded latent membrane protein 1 (LMP1) may trigger the transcription factor AP-1 including c-Jun and c-fos. In this report, using a Tet-on LMP1 HNE2 cell line which is a dual-stable LMP1 integrated nasopharyngeal carcinoma (NPC) cell line and the expression of LMP1 in which could be regulated by the Tet-on system, we show that Jun B can efficiently form a new heterodimeric complex with the c-Jun protein under the regulation of LMP1, phosphorylation of c-Jun (ser 63, ser 73) and Jun B is involved in the process of the new heterodimeric formation. We also find that this heterodimeric form can bind to the AP-1 consensus sequence. Transfection studies suggest that JNK interaction protein (JIP) could inhibit the heterodimer formation of c-Jun and Jun B through blocking the AP-1 signaling pathway triggered by LMP1. The interaction and function between c-Jun protein and Jun B protein increase the repertoire of possible regulatory complexes by LMP1 that could play an important role in the regulation of transcription of specific cellular genes in the process of genesis of nasopharyngeal carcinoma.展开更多
To the Editor:Extranodal natural killer/T-cell lymphoma(ENKTCL)is a highly aggressive lymphoma,closely associated with Epstein–Barr virus(EBV)infection.By using the combination of radiotherapy(RT)and asparaginase-bas...To the Editor:Extranodal natural killer/T-cell lymphoma(ENKTCL)is a highly aggressive lymphoma,closely associated with Epstein–Barr virus(EBV)infection.By using the combination of radiotherapy(RT)and asparaginase-based chemotherapy,more than 70%of patients with early stage ENKTCL have been cured.[1]However,great challenges exist among patients at newly diagnosed advanced stage or relapsed/refractory ENKTCL.展开更多
Abstract:Objective To elucidate the mechanisms by which Epstein-Barr virus-encoded latent membrane protein 1 activates NF-κB in nasopharyngeal carcinoma cells.Methods A tetracycline-regulated LMP1-expressing nasophar...Abstract:Objective To elucidate the mechanisms by which Epstein-Barr virus-encoded latent membrane protein 1 activates NF-κB in nasopharyngeal carcinoma cells.Methods A tetracycline-regulated LMP1-expressing nasopharyngeal carcinoma cell line, Tet-on-LMP1-HNE2, was used as the cell model. The kinetics of the expression of proteins, including LMP1, IκBα and IκBβ, was analyzed by Western blotting. The subcellular localization of NF-κB (p65) was detected by indirect immunofluorescence assay. The NF-κB transactivity was studied by transient transfection and reporter gene assay. Results IκBα was phosphorylated and degraded after the inducible expression of LMP1, although the total protein levels remained stable. The steady-state level of total IκBβ protein may have resulted from the initiation of an autoregulation loop after the activation of NF-κB. No change in the IκBβ level was detected. NF-κB (p65) was translocated from the cytoplasm to the nucleus following degradation of IκBα. After the introduction of the dominant-negative mutant of IκBα (Del 71) into Tet-on-LMP1-HNE2 cells, both nuclear translocation and transactivation of NF-κB induced by LMP1 was significantly inhibited. Conclusions The results indicated that in nasopharyngeal carcinoma cells, LMP1 activated NF-κB via phosphorylation and degradation of IκBα, but not IκBβ. The dominant-negative mutant of IκBα (Del 71) could completely inhibit both the nuclear translocation and transactivation of NF-κB induced by LMP1.展开更多
ObjectiveTo study the effects of dendritic cells (DC) transfected with recombinant vaccinia virus encoding Epstein Barr virus (EBV) latent membrane protein 2A(LMP2A) gene,and to provide evidence for further investiga...ObjectiveTo study the effects of dendritic cells (DC) transfected with recombinant vaccinia virus encoding Epstein Barr virus (EBV) latent membrane protein 2A(LMP2A) gene,and to provide evidence for further investigation on the therapeutic vaccines against EBV associated malignancies. MethodsMature DC were transfected with EBV LMP2A recombinant vaccinia virus (rVV LMP2A). Before and after the transfection,the expression of surface antigens on mature DC including CD1a,CD83,CD40,CD80,HLA DR was measured by fluorescence activated cell sorter (FACS) and the function of DC to stimulate allogeneic T cells proliferation was measured by mixed leukocyte reactions (MLR). ResultsLMP2A protein was highly expressed (66.1 %) in DC after the transfection of rVV LMP2A. No significant changes in the primary surface antigens expression and in the MLR were detected during the transfection. Transfected DC still had strong potential in stimulating the proliferation of allogeneic T cells. ConclusionRecombinant vaccinia virus was an effective and non perturbing vector to mediate the transfection of LMP2A into DC. The functions of mature DC were not affected significantly by the transfection of Vac LMP2A. This study could provide evidence for the further immunotherapy of EBV associated malignancies,e.g. nasopharyngeal carcinoma (NPC).展开更多
Liver transplantation has emerged as a life-saving treatment for several patients with acute liver failure, end stage liver disease and primary hepatic malignancies. However, long term immunosuppressive therapy aiming...Liver transplantation has emerged as a life-saving treatment for several patients with acute liver failure, end stage liver disease and primary hepatic malignancies. However, long term immunosuppressive therapy aiming to reduce the risk of transplant rejection increases the incidence of several com-plications including malignancies. This is illustrated by the observation of a high ratio between observed and expected cases of lymphoproliferative disorders following liver transplantation. Despite a huge heterogeneity in morphological appearance of these disorders ranging from reactive-like lesions to real lymphomas, they are collectively termed posttransplant lymphoproliferative disorders. In this review we will provide an overview of this rare but challenging disorder as a complication of liver transplantation.展开更多
基金StateKeyBasicResearchProgram FundamentalInvestigationonHumanCarcinogenesis (No .G19980 5 12 0 1) +1 种基金NationalScienceFundforDistinguishedYoungScholars (No .3 95 2 5 0 2 2 ) theNationalNaturalScienceFoundationofChina (No 3 0 10 0 0 0 5 )
文摘Objectives To identify whether Epstein Barr virus (EBV) encoded latent membrane protein 1 (LMP1) can induce tumor necrosis factor receptor associated factor 1 (TRAF1) expression and promote its anti apoptosis activity via the NF κB signaling pathway, and assess that LMP1 suppresses apoptosis in nasopharyngeal carcinoma (NPC) Methods A stable transfected cell line HNE2 LMP1 was established by introducing LMP1 cDNA into HNE2 cells Transactivation of TRAF1 was determined by luciferase reporter assay, while expression of TRAF1 mRNA was detected by RT PCR and expression of TRAF1 protein and caspase 3 by Western blot analysis Apoptosis activity was observed through fluorescence staining Results LMP1 induced TRAF1 expression in NPC cells and caused a decrease in apoptosis This induction could be blocked by antisense LMP1 Moreover, LMP1 mediated induction of a TRAF1 promoter driven reporter gene was significantly impaired when the κB site κB1 or κB5 was disrupted, whereas mutation of κB3 had only a minor effect on LMP1 dependent up regulation of the reporter gene Conclusion LMP1 induces TRAF1 expression and promotes its anti apoptosis activity via the NF κB signaling pathway, which may be one of the mechanisms that LMP1 uses to suppress apoptosis in NPC cells
文摘AIM:To verify the methylation status of CDH1, DAPK, COX2, hMLH1 and CDKN2A genes and to evaluate their association with Helicobacter pylori (H. pylori)-cagA+ and Epstein Barr virus (EBV) infections in gastric adenocarcinomas.METHODS: Methylation-specific PCR (MSP) assay was performed in 89 primary gastric carcinomas (intestinal and diffuse types). Microsatellite instability (MSI) analysis was performed using the BAT26 primer set and PCR products were analyzed with the ABI PRISM 3100 Genetic Analyzer using Genescan 3.7 software (Applied Biosystems). Detection of H. pylori and genotyping were performed by PCR, using specifi c primers for ureaseC and cagA genes. The presence of EBV was assessed by in situ hybridization. Statistical analyses were performed using the χ2 or Fisher's exact test.RESULTS: The most frequent hypermethylated gene was COX-2 (63.5%) followed by DAPK (55.7%), CDH1 (51%), CDKN2A (36%) and hMLH1 (30.3%). Intestinal and diffuse adenocarcinomas showed different methylation profiles and there was an association between methylation of E-CDH1 and H. pylori-cagA+ in the intestinal adenocarcinoma type. MSI was correlated with hMLH1 methylation. There was an inverse correlation between DAPK hypermethylation and MSI.CONCLUSION: We found a strong association between CDH1 methylation and H. pylori-cagA+ in intestinal-type gastric cancer, association of MSI and better prognosis and an heterogeneous COX-2 overexpression.
文摘Although many studies have found a kind of a relationship between an Epstein-Barr Virus (EBV) and the development of Multiple Sclerosis (MS), a fundamental aspect of this relationship remains uncertain. What is the cause of Multiple Sclerosis (MS)? In this study, we re-analysed the data as published by Wandinger et al. and were able to establish a new insight: without an Epstein-Barr Virus (EBV) infection no development of Multiple Sclerosis (MS). Furthermore, we determined a highly significant causal relationship between Epstein-Barr Virus (EBV) and multiple sclerosis. Altogether, Epstein-Barr Virus (EBV) is the cause of multiple sclerosis (p-value 0.0004251570).
文摘Objective To detect whether Epstein Barr virus (EBV) harbors in nasopharyngeal lymphoid hyperplasia (NPLH) which is frequently to be seen in Guangzhou, a high incidence area of nasopharyngeal carcinoma (NPC), and to explore the relation between NPLH and development of NPC Methods Twenty four 10% formalin fixed, paraffin embedded biopsies oef patients with NPLH and elevated serum IgA antibody titer (≥1∶20) against viral capsid antigen of EB virus (IgA/VCA) were collected from the archives of the Department of Pathology, Sun Yat sen University of Medical Sciences during the period of January to June, 1993 PCR plus Southern blotting hybridization for detection of EBV DNA W fragment and in situ hybridization for detection of EB virus encoded small RNAs (EBERs) were performed All the patients were followed up more than 5 years Results Twenty two of 24 (91 7%) NPLH tissues contained EBV DNA A few definitely EBERs positive B lymphocytes could be found in 17 out of 24 specimens (70 8%) Neither NPC nor any EBV associated malignancies were developed in all of these 24 patients up to date Conclusion Most of the NPLH tissues taken from the patients with an elevated serum IgA/VCA titer carry EBV, which is harbouring in the nuclei of a few infiltrating and hyperplastic B lymphocytes The NPLH without epithelial dysplasia can not be recognized as a precancerous lesion, and EBV infection in these lesions is not an important event, having no substantial significance in development of NPC
文摘Epstein Barr virus （EBV） positive mucocutaneous ulcers（EBVMCU） form part of a spectrum of EBV-associatedlymphoproliferative disease. They have been reportedin the setting of immunosenescence and iatrogenicimmunosuppression, affecting the oropharyngeal mucosa,skin and gastrointestinal tract （GIT）. Case reports andseries to date suggest a benign natural history respondingto conservative management, particularly in the GIT. Wereport an unusual case of EBVMCU in the colon, arisingin the setting of immunosuppression in the treatment ofCrohn＇s disease, with progression to Hodgkin lymphoma18 mo after cessation of infliximab. The patient presentedwith multiple areas of segmental colonic ulceration,histologically showing a polymorphous infiltrate withEBV positive Reed-Sternberg-like cells. A diagnosisof EBVMCU was made. The ulcers failed to regressupon cessation of infliximab and methotrexate for 18mo. Following commencement of prednisolone for herCrohn＇s disease, the patient developed widespreadHodgkin lymphoma which ultimately presented as alife-threatening lower GIT bleed requiring emergencycolectomy. This is the first report of progression ofEBVMCU to Hodgkin lymphoma, in the setting of ongoingiatrogenic immunosuppression and inflammatory boweldisease.
基金supported by grants from the National Key Research and Development Program of China(2022YFC3400900)Postdoctoral Fellowship Program of CPSF(GZB20230886)+3 种基金Chinese Postdoctoral Science Foundation(2023M743998)Natural Science Foundation of China(82030046)the Program for Guangdong Introducing Innovative and Entrepreneurial Teams(2019BT02Y198)Guangdong Science and Technology Department(2020B1212030004).
文摘In a recent study published in Cell,Vietzen and colleagues discovered the novel role of natural killer(NK)cells and EBVspecific CD8+T cell response in controlling EBV-inducing autoimmune response and collectively defined virus and host genetics factors associated with a significantly raised risk of multiple sclerosis.
文摘Epstein-Barr virus (EBV) encoded latent membrane protein 1 (LMP1) may trigger the transcription factor AP-1 including c-Jun and c-fos. In this report, using a Tet-on LMP1 HNE2 cell line which is a dual-stable LMP1 integrated nasopharyngeal carcinoma (NPC) cell line and the expression of LMP1 in which could be regulated by the Tet-on system, we show that Jun B can efficiently form a new heterodimeric complex with the c-Jun protein under the regulation of LMP1, phosphorylation of c-Jun (ser 63, ser 73) and Jun B is involved in the process of the new heterodimeric formation. We also find that this heterodimeric form can bind to the AP-1 consensus sequence. Transfection studies suggest that JNK interaction protein (JIP) could inhibit the heterodimer formation of c-Jun and Jun B through blocking the AP-1 signaling pathway triggered by LMP1. The interaction and function between c-Jun protein and Jun B protein increase the repertoire of possible regulatory complexes by LMP1 that could play an important role in the regulation of transcription of specific cellular genes in the process of genesis of nasopharyngeal carcinoma.
基金National Natural Science Foundation of China(No.82170181)Beijing Hospitals Authority Youth Programme(No.QML20200201)+1 种基金Beijing Natural Science Foundation(No.7222027)CSH Young Scholars and 3SBioPharmaceutical joint research project(No.KYC2201001)
文摘To the Editor:Extranodal natural killer/T-cell lymphoma(ENKTCL)is a highly aggressive lymphoma,closely associated with Epstein–Barr virus(EBV)infection.By using the combination of radiotherapy(RT)and asparaginase-based chemotherapy,more than 70%of patients with early stage ENKTCL have been cured.[1]However,great challenges exist among patients at newly diagnosed advanced stage or relapsed/refractory ENKTCL.
基金ThisprojectwassupportedbytheStateKeyBasicResearchProgram FundamentalInvestigationonHumanCarcinogenesis (No G19980 5 12 0 1) +2 种基金theNationalScienceFundationforDistinguishedYoungScholars (No 395 2 0 2 2 ) andtheChinaMedicalBoardofNewYork Inc (N
文摘Abstract:Objective To elucidate the mechanisms by which Epstein-Barr virus-encoded latent membrane protein 1 activates NF-κB in nasopharyngeal carcinoma cells.Methods A tetracycline-regulated LMP1-expressing nasopharyngeal carcinoma cell line, Tet-on-LMP1-HNE2, was used as the cell model. The kinetics of the expression of proteins, including LMP1, IκBα and IκBβ, was analyzed by Western blotting. The subcellular localization of NF-κB (p65) was detected by indirect immunofluorescence assay. The NF-κB transactivity was studied by transient transfection and reporter gene assay. Results IκBα was phosphorylated and degraded after the inducible expression of LMP1, although the total protein levels remained stable. The steady-state level of total IκBβ protein may have resulted from the initiation of an autoregulation loop after the activation of NF-κB. No change in the IκBβ level was detected. NF-κB (p65) was translocated from the cytoplasm to the nucleus following degradation of IκBα. After the introduction of the dominant-negative mutant of IκBα (Del 71) into Tet-on-LMP1-HNE2 cells, both nuclear translocation and transactivation of NF-κB induced by LMP1 was significantly inhibited. Conclusions The results indicated that in nasopharyngeal carcinoma cells, LMP1 activated NF-κB via phosphorylation and degradation of IκBα, but not IκBβ. The dominant-negative mutant of IκBα (Del 71) could completely inhibit both the nuclear translocation and transactivation of NF-κB induced by LMP1.
基金This paper is supported by grant from the National Natural Science Foundation of China(No.30 1 70 880 )
文摘ObjectiveTo study the effects of dendritic cells (DC) transfected with recombinant vaccinia virus encoding Epstein Barr virus (EBV) latent membrane protein 2A(LMP2A) gene,and to provide evidence for further investigation on the therapeutic vaccines against EBV associated malignancies. MethodsMature DC were transfected with EBV LMP2A recombinant vaccinia virus (rVV LMP2A). Before and after the transfection,the expression of surface antigens on mature DC including CD1a,CD83,CD40,CD80,HLA DR was measured by fluorescence activated cell sorter (FACS) and the function of DC to stimulate allogeneic T cells proliferation was measured by mixed leukocyte reactions (MLR). ResultsLMP2A protein was highly expressed (66.1 %) in DC after the transfection of rVV LMP2A. No significant changes in the primary surface antigens expression and in the MLR were detected during the transfection. Transfected DC still had strong potential in stimulating the proliferation of allogeneic T cells. ConclusionRecombinant vaccinia virus was an effective and non perturbing vector to mediate the transfection of LMP2A into DC. The functions of mature DC were not affected significantly by the transfection of Vac LMP2A. This study could provide evidence for the further immunotherapy of EBV associated malignancies,e.g. nasopharyngeal carcinoma (NPC).
文摘Liver transplantation has emerged as a life-saving treatment for several patients with acute liver failure, end stage liver disease and primary hepatic malignancies. However, long term immunosuppressive therapy aiming to reduce the risk of transplant rejection increases the incidence of several com-plications including malignancies. This is illustrated by the observation of a high ratio between observed and expected cases of lymphoproliferative disorders following liver transplantation. Despite a huge heterogeneity in morphological appearance of these disorders ranging from reactive-like lesions to real lymphomas, they are collectively termed posttransplant lymphoproliferative disorders. In this review we will provide an overview of this rare but challenging disorder as a complication of liver transplantation.
