Gastric Cancer
Copyright ©2005 Baishideng Publishing Group Inc.
World J Gastroenterol. Feb 7, 2005; 11(5): 629-633
Published online Feb 7, 2005. doi: 10.3748/wjg.v11.i5.629
Figure 1
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Figure 1 In situ hybridization for EBER1 in gastric carcinoma tissue. A: In situ EBER1 hybridization with antisense probes. Strong signals were observed in the nuclei of all tumor cells; B: In situ EBER1 hybridization with sense probes; C: Hematoxylin/eosin (H&E) staining in the adjacent pair of EBER1 in situ hybridization. original magnification ×200.
Figure 2
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Figure 2 RT-PCR and Southern hybridization analysis of EBNA gene transcription using promoters. M: DIG-labeled DNA molecular weight marker VIII (Roche). Lane 1: EBV-positive LCL(positive control); lane 2: EBV-negative Ramos cells(negative control); lanes 3-13: EBV-positive gastric carcinoma samples. GAPDH mRNA was amplified to check pertinent RNA extraction and results were shown by EB staining.
Figure 3
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Figure 3 Detection of EBV latent gene expression (A) and EBV lytic gene expression (B) by RT-PCR and Southern hybridization. M: DIG-labeled DNA molecular weight marker VIII (Roche). Lane 1: EBV-positive LCL (positive control); lane 2: EBV-negative Ramos cells (negative control); lanes 3-13: EBV-positive gastric carcinoma samples. GAPDH mRNA was amplified to check pertinent RNA extraction and results were shown by EB staining.