Graduate Institute of Microbiology and Immunology , National Yang-Ming Medical College , Taipei , Taiwan , Republic of China .
Chung Hua Min Kuo Wei Sheng Wu Chi Mien I Hsueh Tsa Chih 25 : 59-68 ( 1992)
Abstract
To study the oncogenesis of human esophageal carcinoma , the presence of DNA sequences homologous to several DNA tumor viruses and the expression of oncogenes and growth factor genes were examined in two esophageal carcinoma cell lines of Chinese origin , CE48T/VGH and CE81T/VGH .
Southern blot analyses failed to detect sequences homologous to hepatitis B virus ( HBV ) , Epstein-Barr virus ( EBV ) , herpes simplex virus type 2 ( HSV-2 ) , cytomegalovirus ( CMV ) or human papilloma virus ( HPV ) genomes .
Northern blot analyses revealed that c-myc , c-src , c-H-ras , c-abl , c-sis , and p53 genes were expressed .
In addition , transcripts of transforming growth factor alpha ( TGF alpha ) , TGF beta , and platelet derived growth factor A ( PDGF A ) genes were detected .
These studies suggest that DNA tumor viruses may not be involved in the carcinogenesis of esophageal carcinoma .
However , cooperation among different oncogenes and the production of growth factors may play an important role in that carcinogenesis .
Gene Symbols
Chemical Identifiers ( Names)
Third Department of Internal Medicine , Fukui Medical School , Japan .
J Cardiovasc Pharmacol 20 : 900-6 ( 1992)
Abstract
Cilostazol , a cyclic AMP phosphodiesterase inhibitor , has been used as an antiplatelet agent .
In the present study , we investigated the in vitro effect of cilostazol on DNA synthesis in rat aortic arterial smooth muscle cells ( SMCs ) in culture stimulated with fetal calf serum ( FCS ) , platelet-derived growth factor ( PDGF ) , insulin , or insulin-like growth factor-I ( IGF-I ) .
Micromolar concentrations of cilostazol inhibited [ 3H]thymidine incorporation into DNA and cell growth as determined by cell number and protein concentration .
Treatment with cilostazol increased the intracellular concentration of cyclic AMP , suggesting that the inhibition of SMC proliferation by cilostazol may be mediated through increased levels of cyclic AMP .
The results suggested that cilostazol , by interfering with the proliferation of arterial SMCs , may have potential to prevent initiation and progression of atherosclerosis .