Highly frequent homozygous deletion of the p16 gene in esophageal cancer cell lines.
To study the involvement of the p16 tumor suppressor gene in esophageal cancer development, we examined homozygous deletion of the p16 gene in 13 human esophageal cancer cell lines and 9 gastric cancer cell lines, in which some of genetic alterations have already been characterized. By Southern blot analysis, homozygous deletion was observed in 12 out of the 13 esophageal cancer cell lines (92%), in 2 out of a total of 9 gastric cancer cell lines (22%). It was also found that the p16 gene loss, cyclin D1 amplification and p53 gene mutations occurred independently in these cell lines. These findings suggest that loss or mutations of the p16 gene are involved in most esophageal cancers and that mutation of this gene plays a critical role in the development of esophageal cancer.
Igaki
H
H
Genetics Division, National Cancer Center Research Institute, Tokyo, Japan.
Sasaki
H
H
Kishi
T
T
Sakamoto
H
H
Tachimori
Y
Y
Kato
H
H
Watanabe
H
H
Sugimura
T
T
Terada
M
M
D015139:Blotting, Southern; D002352:Carrier Proteins / Q000235:genetics*; D019938:Cyclin D1; D019941:Cyclin-Dependent Kinase Inhibitor p16; D016213:Cyclins / Q000235:genetics; D004938:Esophageal Neoplasms / Q000235:genetics*; D017353:Gene Deletion; D016158:Genes, p53; D006720:Homozygote; D006801:Humans; D009154:Mutation; D015513:Oncogene Proteins / Q000235:genetics; D047428:Protein Kinase Inhibitors; D013274:Stomach Neoplasms / Q000235:genetics; D014407:Tumor Cells, Cultured
D002352:Carrier Proteins; D019941:Cyclin-Dependent Kinase Inhibitor p16; D016213:Cyclins; D015513:Oncogene Proteins; D047428:Protein Kinase Inhibitors; D019938:Cyclin D1