Selective gene expression using a DF3/MUC1 promoter in a human esophageal adenocarcinoma model

In vivo Radioiodide Imaging and Treatment of Pancreatic Cancer Xenografts after MUC1 Promoter-Driven Expression of the Human Sodium-Iodide Symporter

“…MUC1 overexpression is associated with increased metastatic potential and poor patient survival [15,16] , so this construct has a potential for application in the MUC1 overexpression tumor model. Previous studies have shown that the 1.4-kb 5 -MUC1 fragment cloned from human breast cancer cells had been successfully used to drive the expression of therapeutic genes in tumor tissues overexpressing the protein [17][18][19][20] . It is also known that the 0.8-kb Sac I/ Xmn I fragment, located at the 3 end of the MUC1 promoter, is a minimal functional fragment that can direct transcription of the test genes at maximal levels [21,22] .…”

Effectiveness of HSV-tk Suicide Gene Therapy Driven by the Grp78 Stress-Inducible Promoter in Esophagogastric Junction and Gastric Adenocarcinomas

“…11,12,22 Heideman et al 13 investigated the epithelial cell adhesion molecule (EpCAM) as a gene therapy target using cell lines (TE-1 and TE-2) that have been shown to be derived from an esophageal squamous cell carcinoma rather than an esophageal adenocarcinoma. Further demonstrating the poor availability of suitable esophageal adenocarcinoma cell lines, Gupta et al 10 1 and 8). Fifteen-and 1,500-bp markers are also shown, as well as non-specific PCR products (probably primer dimers) at 54 bp.…”

“…8 The limited number of esophageal adenocarcinoma gene therapy studies have unfortunately mostly used inappropriate cell lines or animal models, reflecting the paucity of suitable models. [10][11][12][13][14] There have been many gastric cancer gene therapy studies with significant progress, if only at the preclinical stage, 8 but none using the promising HSV-tk/GCV approach with the Grp78 promoter as in the current study.…”

The Role of Glycogen Synthase Kinase 3-β in Immunity and Cell Cycle: Implications in Esophageal Cancer

“…Using various human EC cell lines, Saito et al (1994a) reported the significant antitumor effects of recombinant human TNF. Moreover, increased TNF was reported to enhance the radiosensitivity of EC patients by interacting with ionizing radiation and subsequently produced greater tumor regression and a delay in tumor regrowth (Gupta et al 2003). In contrast to the anti-EC effects of TNF, there are also several reports that have shown that TNF can promote EC via enhancing expression of oncogenes like c-Myc and b-catenin (Tselepis et al 2002).…”