A Rapid and Reliable Enzyme Immunoassay PCR-Based Screening Method to Identify EBV-Carrying Gastric Carcinomas

Beek, Josine van; Hausen, Axel zur; Kranenbarg, E. Klein; Warring, Ralph J; Bloemena, Elisabeth; Craanen, M. E.; Velde, Cornelis J.H. van de; Middeldorp, Jaap M.; Meijer, Chris J.L.M.; Brule, Adriaan J. C. van den

doi:10.1097/01.mp.0000024147.43288.b1

Cited by 19 publications

(17 citation statements)

References 34 publications

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“…GC tumor biopsy specimens were obtained from the archives of the VU University Medical Center, Amsterdam, and have been described in earlier studies (40,41). Sections of these tumors were analyzed for the presence of EBV-encoded RNAs (EBERs) by EBER in situ hybridization (EBERish) as described previously (42).…”

Section: Methodsmentioning

confidence: 99%

Contributions of the Epstein-Barr Virus EBNA1 Protein to Gastric Carcinoma

Sivachandran

Dawson

Young

et al. 2012

J Virol

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Approximately 10% of gastric carcinomas (GC) are comprised of cells latently infected with Epstein-Barr virus (EBV); however, the mechanism by which EBV contributes to the development of this malignancy is unclear. We have investigated the cellular effects of the only EBV nuclear protein expressed in GC, EBNA1, focusing on promyelocytic leukemia (PML) nuclear bodies (NBs), which play important roles in apoptosis, p53 activation, and tumor suppression. AGS GC cells infected with EBV were found to contain fewer PML NBs and less PML protein than the parental EBV-negative AGS cells, and these levels were restored by silencing EBNA1. Conversely, EBNA1 expression was sufficient to induce the loss of PML NBs and proteins in AGS cells. Consistent with PML functions, EBNA1 expression decreased p53 activation and apoptosis in response to DNA damage and resulted in increased cell survival. In addition, EBNA1 mutants unable to bind CK2 kinase or ubiquitin-specific protease 7 had decreased ability to induce PML loss and to interfere with p53 activation. PML levels in EBV-positive and EBV-negative GC biopsy specimens were then compared by immunohistochemistry. Consistent with the results in the AGS cells, EBV-positive tumors had significantly lower PML levels than EBV-negative tumors. The results indicate that EBV infection of GC cells leads to loss of PML NBs through the action of EBNA1, resulting in impaired responses to DNA damage and promotion of cell survival. Therefore, PML disruption by EBNA1 is one mechanism by which EBV may contribute to the development of gastric cancer.

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Section: Methodsmentioning

confidence: 99%

Contributions of the Epstein-Barr Virus EBNA1 Protein to Gastric Carcinoma

Sivachandran

Dawson

Young

et al. 2012

J Virol

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“…GC is one of the most common carcinomas globally, and recent studies revealed the association of EBV with about 10% of GC cases worldwide (Burke et al, 1990;Shibata and Weiss, 1992;Takada, 2000;van Beek et al, 2002). However, the influence of EBV infection on GC development and treatment is still unclear.…”

Section: Introductionmentioning

confidence: 99%

Association between Epstein-Barr Virus Infection and Chemoresistance to Docetaxel in Gastric Carcinoma

Shin

Kim

Lee

2011

Molecules and Cells

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Epstein-Barr virus (EBV) is associated with human cancers such as nasopharyngeal carcinoma, Burkitt's lymphoma, Hodgkin's disease, and gastric carcinoma (GC). EBV is associated with about 10% of all GC cases globally. EBV-associated GC has distinct features from EBV-negative GC. However, it is still unclear if EBV infection has any effect on GC chemoresistance. Cell proliferation assay, cell cycle analysis, and active caspase Western blot revealed that the EBV-positive GC cell line (AGS-EBV) showed chemoresistance to docetaxel compared to the EBV-negative GC cell line (AGS). Docetaxel treatment increased expression of Bax similarly in AGS and AGS-EBV cell lines. However, Bcl-2 induction was markedly higher in AGS-EBV cells, after docetaxel treatment. Although docetaxel increased the expression of p53 to a similar extent in both cell lines, induction of p21 in AGS-EBV cells was lower than in AGS cells. Furthermore, expression of survivin was higher in AGS-EBV cells than in AGS cells following docetaxel treatment as well as at basal state. EBVlytic gene expression was induced by docetaxel treatment in AGS-EBV cells. The results suggest that EBV infection and lytic induction confers chemoresistance to GC, possibly by regulating cellular and EBV latent and lytic gene expression.

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“…The MeningoFinder assay was compared to routine in-house PCRs. The PCRs for enterovirus, HSV-1, HSV-2, and VZV were performed by PAMM (1,6,15), and the PCRs for CMV and EBV were performed at the Laboratory of Medical Microbiology at the Maastricht University Medical Center (MUMC) (10,16). Viral RNA/DNA from clinical samples (200-l cerebrospinal fluid specimens) for PCR or MLPA was isolated using either the Nuclisense easyMAG (bioMerieux, Boxtel, The Netherlands) or the MagnaPure LC nucleic acid system (Roche Diagnostics) according to the manufacturers' instructions.…”

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confidence: 99%