B cell clonality in gastric lymphoid tissues of patients with Sjogren's syndrome.

Ferraccioli, Gianfranco; Sorrentino, Dario; Vita, Salvatore De; Casatta, L.; Labombarda, Antonella; Avellini, Claudio; Dolcetti, Riccardo; Luca, Dario Di; Ca, Beltrami; Boiocchi, Mauro; Bartoli, Ettore

doi:10.1136/ard.55.5.311

Cited by 50 publications

(22 citation statements)

References 28 publications

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“…For example, Epstein Barr virus has been implicated in the genesis of gastric carcinoma [Pagano, 1999, Herrera-Goepfert et al, 1999; herpes simplex virus and human cytomegalovirus have been occasionally associated to gastritis [Nelson andCrippin 1997, Zucker et al, 1994]. Gastric biopsies of patients with Sjo Ègren's syndrome may harbour EBV and HHV-6 DNA [Ferraccioli et al, 1996]. These observations suggested the opportunity to examine gastritis specimens for the presence of HHV-7.…”

Section: Discussionmentioning

confidence: 95%

“…Also, eradication of H. pylori does not necessarily lead to relief of clinical symptoms [Talley et al, 1999]. Second, the presence of herpesvirus DNA, in particular Epstein Barr virus (EBV) and human herpesvirus 6 (HHV-6), was reported in, respectively, 10% and 14% of gastric tissues [Ferraccioli et al, 1996]. The presence of HHV-6 in the gastric mucosa suggested the opportunity to extend the analysis to HHV-7, which is related closely to HHV-6 [Berneman et al, 1992;Nicholas, 1996;Megaw et al, 1998] and more prevalent in the human population [Di Luca et al, 1995b].…”

Section: Introductionmentioning

confidence: 99%

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Human herpesvirus 7 is latent in gastric mucosa

et al. 2001

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Chronic gastritis is associated frequently with persistent infection by Helicobacter pylori. However, not all patients with chronic gastritis have evidence of H. pylori infection, suggesting that other factors might contribute to the development of gastritis. The present study was undertaken to evaluate a possible etiologic role of human herpesvirus 7 (HHV-7). HHV-7 DNA was detected in about 80% of gastric biopsies, both in healthy mucosa from individuals without evidence of inflammation and in biopsies from patients with histologically confirmed chronic gastric inflammation. HHV-7 was present also in H. pylori negative samples, was associated specifically with gastric tissue and not with residual blood within the mucosa, and was present with high viral loads. HHV-7 DNA persisted in several patients also after remission of gastric inflammation and the viral presence did not correlate with specific symptoms. Analysis by RT-PCR showed that HHV-7 is transcriptionally inactive in chronic gastritis lesions. These observations show that gastric tissue represents a site of HHV-7 latent infection and a potential reservoir for viral reactivation.

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Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

Human herpesvirus 7 is latent in gastric mucosa

et al. 2001

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“…These organs are normally devoid of organized lymphoid tissue and lymphoma. MALT lymphomas arise from these sites as a result of chronic inflammatory or autoimmune disorders, such as H. pylori-associated chronic gastritis, lymphoepithelial sialoadenitis, Sjögren syndrome and Hashimoto thyroiditis (8,9). The common karyotypic alterations that characterize MALT lymphoma include the trisomies of 3 and 18 (10,11) and the translocations t(11;18) (q21;q21) (12,13), t(1;14)(p22;q32) (14,15), t(14;18)(q32;q21) (10,16), and t(3;14)(p14.1;q32) (17,18), which commonly activate the NF-κB pathway.…”

Section: Introductionmentioning

confidence: 99%

Accumulation of aberrant CpG hypermethylation by Helicobacter pylori infection promotes development and progression of gastric MALT lymphoma

Oka¹

2009

Int J Oncol

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Abstract. Aberrant DNA hypermethylation is an important mechanism for the inactivation of tumor-related genes in human tumors. Gastric mucosa-associated lymphoid tissue (MALT) lymphomas arise from Helicobacter pylori-associated chronic gastritis; most patients are H. pylori-positive and eradication therapy is highly effective. In the present study, we used methylation-specific PCR to analyze the DNA methylation status of 11 tumor-related genes (Kip2, p16, p15, p73, MGMT, DAPK, MINT1, MINT2, MINT31 and HCAD) in 21 specimens of MALT lymphoma, 5 specimens of MALT lymphoma with large cell component (high-grade MALT lymphoma), 15 specimens of diffuse large B-cell lymphoma (DLBCL), 8 specimens of complete remission of MALT lymphoma after eradication therapy, 5 specimens with no evidence of malignancy and PBMCs from 10 healthy donors. The average number of methylated genes was significantly greater in gastric lymphomas as compared to normal controls (P<0.001). The CpG island methylator phenotype (CIMP) was observed in 93.3% (14/15) of DLBCLs, 100% (5/5) of high-grade MALT lymphomas and 61.9% (13/21) of MALT lymphomas; in contrast, CIMP was not found in the control group (0%). The average number of methylated genes and the CIMP incidence significantly increased with H. pylori infection. Furthermore, aberrant CpG methylation of specific genes, such as p16, MGMT and MINT31, was consistently associated with H. pylori infection. These findings strongly suggest that H. pylori infection causes the aberrant DNA hypermethylation of specific genes and induces CIMP, which is an important epigenetic mechanism for the development and progression of gastric MALT lymphoma; additionally, our findings provide new epigenetic markers.

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“…8,9,12,13 Autoimmunity may contribute to gastric chronic inflammation and lymphoproliferation. 11,[14][15][16][17][18][19] In particular, studies on SS-related chronic gastritis and gastric low-grade B-cell NHL showed intragastric B-cell clonal expansion also in the absence of HP infection. 11,18,19 Furthermore, recent clinical and experimental results have linked the HCV to SS-like manifestations and acquisition of MALT.…”

mentioning

confidence: 99%

“…11,[14][15][16][17][18][19] In particular, studies on SS-related chronic gastritis and gastric low-grade B-cell NHL showed intragastric B-cell clonal expansion also in the absence of HP infection. 11,18,19 Furthermore, recent clinical and experimental results have linked the HCV to SS-like manifestations and acquisition of MALT. 2,[20][21][22] We herein report the gastric mucosa as a possible extrahepatic localization of HCV.…”

mentioning

confidence: 99%

Gastric mucosa as an additional extrahepatic localization of hepatitis C virus: Viral detection in gastric low-grade lymphoma associated with autoimmune disease and in chronic gastritis

Vita

Sansonno

et al. 2000

Hepatology

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Hepatitis C virus (HCV) has been localized in several tissues besides the liver. 1 The definition of the possible extrahepatic localizations of the virus may be relevant to better address the issue of some of the extrahepatic manifestations of chronic HCV infection. As regards the gastric microenvironment, gastric lymphoma has been reported in patients with HCV infection, 2-6 and a relationship was noticed between HCV infection and B-cell clonal expansion in chronic gastritis lesions in Sjö gren' s syndrome (SS). 7 At present, local infection by Helicobacter pylori (HP) in the gastric mucosa is considered a crucial step for the development of chronic gastritis and gastric low-grade B-cell non-Hodgkin' s lymphoma (NHL) of mucosa-associated lymphoid tissue (MALT). [8][9][10] However, important issues regarding the pathobiology of HP-related gastric lymphoproliferation are still ill-defined, such as the definition of additional pathogenetic events implicated in the malignant transformation (nearly all the HP-infected individuals do not develop a gastric lymphoma), the possible lack of regression of HPassociated gastric lymphoproliferation after HP eradication, [8][9][10][11] and the evidence of gastric low-grade B-cell NHLs, which appear HP-negative ab initio. 8,9,12,13 Autoimmunity may contribute to gastric chronic inflammation and lymphoproliferation. 11,[14][15][16][17][18][19] In particular, studies on SS-related chronic gastritis and gastric low-grade B-cell NHL showed intragastric B-cell clonal expansion also in the absence of HP infection. 11,18,19 Furthermore, recent clinical and experimental results have linked the HCV to SS-like manifestations and acquisition of MALT. 2,[20][21][22] We herein report the gastric mucosa as a possible extrahepatic localization of HCV. Viral antigens and RNA were detected within a HP-positive low-grade B-cell NHL lesion, in an HCV-infected patient with clinical and pathological findings consistent with SS. This gastric low-grade B-cell NHL did not regress, despite successful HP eradication. Molecular analyses of the immunoglobulin heavy chain (IgH) genes used by the neoplastic clone indicated an antigen-driven

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B cell clonality in gastric lymphoid tissues of patients with Sjogren's syndrome.

Abstract: 1996; 55: 311-316)

Cited by 50 publications

References 28 publications

Human herpesvirus 7 is latent in gastric mucosa

Human herpesvirus 7 is latent in gastric mucosa

Accumulation of aberrant CpG hypermethylation by Helicobacter pylori infection promotes development and progression of gastric MALT lymphoma

Gastric mucosa as an additional extrahepatic localization of hepatitis C virus: Viral detection in gastric low-grade lymphoma associated with autoimmune disease and in chronic gastritis

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