Liver Cancer
Copyright ©The Author(s) 2004.
World J Gastroenterol. Mar 1, 2004; 10(5): 638-642
Published online Mar 1, 2004. doi: 10.3748/wjg.v10.i5.638
Figure 1
Figure 1 Corresponding distribution of hTERT signals and c-Myc staining in HCC tissue detected by HE staining (A, D, and G); in situ hybridization (hTERT positive, B and H; hTERT negative, E); and immunohistochemistry (c-Myc positive, C and F; c-Myc negative, I).
Figure 2
Figure 2 A: Schematic diagram of LUC reporter plasmids. Pro-moter fragments of decreasing size from the 5’ end (1375 bp, 776 bp, 100 bp and Myc double deletion mutant hTERT-pro-moter reporter plasmids of 181 bp) upstream of the initiating ATG were inserted into luciferase (LUC) reporter vector pGL3-Basic in sense orientation. +1, the transcription start site. Bind-ing sites for c-Myc/Max and Sp1 are shown. B: Transcription activation of hTERT promoter. Data represent normalized rela-tive luciferase fold activity compared with the promoterless pGL3 basic plasmid.