These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Identification of the expression profile of apoptotic esophageal cancer cells by adenoviral-fragile histidine triad treatment.
    Author: Mimori K, Ishii H, Inoue H, Barnard GF, Mori M.
    Journal: J Gastroenterol Hepatol; 2008 Dec; 23 Suppl 2():S205-9. PubMed ID: 19120899.
    Abstract:
    BACKGROUND: The fragile histidine triad (FHIT) functions as a tumor suppressor, and giving adenoviral-FHIT (Ad-FHIT) is thus expected to be clinically beneficial. Much attention has recently been focused on which genes are commonly regulated by Ad-FHIT, and which genes are dominant in Ad-FHIT-induced apoptotic cells. METHODS: Ad-FHIT apoptosis-induced cells (H1299 and TE4) and non-apoptosis-induced cells (TE2) were used in the current experiments. The total RNA extracted from Ad-FHIT or control was labeled with Cy3-dCTP or Cy5-dCTP and hybridized with 19,192 genes on a chip. A microarray analysis for each gene was carried out with high reproducibility provided by seven independent experiments and duplicated oligos on a chip. RESULTS: We listed the upregulated genes based on the TE4:TE2 expression ratio, such as c-Src, Jak-1, and sialyltransferase, which are expected to be target pathways as well as the downregulated genes, including CASP8 and CASP10, after Ad-FHIT treatment in esophageal cancer. CONCLUSIONS: The current microarray analysis indicated that the apoptosis of esophageal cancer observed after giving Ad-FHIT was possibly induced by activation of the c-Src gene and inactivation of the CASP8 gene.
    [Abstract] [Full Text] [Related] [New Search]