Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.7.1.21 (
thymidine kinase
)
7,561
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Allelic expression was examined by single-strand conformation polymorphism analysis in murine fibrosarcomas from inter-subspecific F1 mice between C57BL/6 and MSM. Ten genes encoding p53, mdm2,
E-cadherin
, 72 kD metalloproteinase and its inhibitor (Timp2),
thymidine kinase
and four glucose transporters (Gluts) were examined. These genes were chosen because of their probable association with tumor development and progression. In some of the tumors and cell lines, p53,
E-cadherin
and Glut3 genes showed remarkable differences in allelic expression, one allele being poorly expressed. The allele-specificity persisted in nine cell lines obtained by repeated transplantations from one tumor. These results suggest that expression of some genes is allele-specific in tumor cells and the pattern of specificity is stable. Such a decrease or a loss of expression in one of the alleles may be functionally equivalent to the loss of heterozygosity of the gene, and therefore this may confer malignant properties on tumor cells. It is also suggested that differential expression of two alleles is a common event in tumor cells.
...
PMID:Difference in allelic expression of genes probably associated with tumor progression in murine fibrosarcomas and cell lines. 796 Nov 3
The
thymidine kinase
/ganciclovir (TK/GCV) cancer gene therapy approach is based on inducing GCV metabolite cytotoxicity in tumor cells expressing the herpes simplex virus TK gene and exposed to GCV. A bystander effect, mediated by gap junctions, accounts for the transfer of toxic metabolites from TK-expressing cells to neighboring cells. It has been proposed that
E-cadherin
participates in the formation and function of such gap junctions. In this study we investigate the influence of
E-cadherin
on TK/GCV suicide therapy with a panel of cellular and in vivo models of pancreatic ductal adenocarcinoma. We observed a strong correlation of
E-cadherin
expression and the TK/GCV bystander effect, associated with the modulation of gap junction communication and connexin expression or localization. Importantly, the co-expression of TK and
E-cadherin
genes in the adenoviral vector AdTat8TKIE improved TK/GCV cytotoxicity and triggered a potent antitumoral effect, superior to standard AdTat8TK/GCV in MIAPaCa-2 xenografts. The increased expression of
E-cadherin
resulted in the reduction of the bcl-2 content. Interestingly, the knockdown of bcl-2 sensitized cells to TK/GCV. Thus, we propose that by restoring
E-cadherin
in pancreatic tumor cells we will improve TK/GCV therapy, both by enhancing the bystander effect and by facilitating the induction of apoptosis.
...
PMID:E-cadherin contributes to the bystander effect of TK/GCV suicide therapy and enhances its antitumoral activity in pancreatic cancer models. 2072 May 74
