[Quantitive detection of multi-gene expressions and DNA content in the precancerous cells of esophageal carcinoma].
OBJECTIVE
To explore the molecular events and mechanism in the carcinogenesis of esophageal epithelium in the high incidence area of esophageal carcinoma.


METHODS
Epithelial cells collected from the high incidence area of esophageal carcinoma were used to detect DNA content and ploidy by propidium iodide(PI) stain. The expressions of p53, p16 and cyclin D1 were stained by indirect immunofluorescence of fluorescein isothiocyanate(FTTC), which were detected by flow cytometry (FCM).


RESULTS
During the process of carcinogenesis, DNA content increased significantly. The diploid cells decreased while heteroploid cells increased sharply, with a heteroploidy rate of 84.2%. At the same time, the p53 protein accumulated and p16 was deleted. The positive rates of p53 and oncogene cyclin D1 were both 100%(5/5, 6/6) in the cancer group.


CONCLUSIONS
In the early carcinogenesis of esophageal epithelium, DNA content and heteroploidy rates increase with tumor suppressor gene p16 deletion and p53 protein accumulation while oncogene cyclin D1 is overexpressed. Multiple molecular events have already occurred when esophageal carcinoma develops.
Zuo
Lianfu
L
Hebei Cancer Institute, Shijiazhuang 050011, China.
Lin
Peizhong
P
Qi
Fengying
F
Zhang
Linxi
L
Guo
Jianwen
J
Liu
Jianghui
J
D019938:Cyclin D1 / Q000378:metabolism; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000378:metabolism; D004273:DNA, Neoplasm / Q000378:metabolism*; D004938:Esophageal Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D005434:Flow Cytometry; D015870:Gene Expression; D006801:Humans; D011230:Precancerous Conditions / Q000235:genetics*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
D019941:Cyclin-Dependent Kinase Inhibitor p16; D004273:DNA, Neoplasm; D016159:Tumor Suppressor Protein p53; D019938:Cyclin D1