TY - JOUR
T1 - Analysis of gene amplification and overexpression in human esophageal‐carcinoma cell lines
AU - Kanda, Yuji
AU - Nishiyama, Yasuyuki
AU - Shimada, Yutaka
AU - Imamura, Masayuki
AU - Nomura, Hiroshi
AU - Hiai, Hiroshi
AU - Fukumoto, Manabu
PY - 1994/7/15
Y1 - 1994/7/15
N2 - Gene amplification/overexpression was analyzed in 23 cell lines derived from human esophageal squamous‐cell‐carcinoma tissues by Southern and Northern hybridizations to c‐myc, c‐erbB, hst‐1 and cyclin‐DI probes. Amplification of the c‐myc gene was observed in 5 cell lines derived from well‐differentiated carcinomas and all of them were accompanied by co‐amplification of other examined oncogenes. The c‐erbB gene was amplified in 3 cell lines. Co‐amplification of hst‐1 and cyclin DI, both of which are located in chromosome 11q13, was found in 9 cell lines. Without exception their amplification was simultaneous and the magnitudes were similar. Their amplification, but not their overexpression, was significantly correlated with poor prognosis in patients from whom the cell lines were established. While hst‐1‐gene expression was not detected, at least 1 of the genes analyzed was overexpressed in 20 cell lines vs. its expression in normal esophageal mucosal tissues. However, gene amplification was not necessarily accompanied by overexpression of the corresponding genes. Expression of the cyclin DI gene, which has been assumed to be a target gene for 11q13 amplification, was not detected in one particular cell line with amplification of 11q13. These results suggest that the amplification/overexpression of more than I oncogene is involved in the carcinogenic process of esophageal carcinoma and that c‐myc‐gene amplification is associated with a well‐differentiated subtype. There remains a possibility that key oncogenes other than cyclin DI are involved in 11q13 amplification.
AB - Gene amplification/overexpression was analyzed in 23 cell lines derived from human esophageal squamous‐cell‐carcinoma tissues by Southern and Northern hybridizations to c‐myc, c‐erbB, hst‐1 and cyclin‐DI probes. Amplification of the c‐myc gene was observed in 5 cell lines derived from well‐differentiated carcinomas and all of them were accompanied by co‐amplification of other examined oncogenes. The c‐erbB gene was amplified in 3 cell lines. Co‐amplification of hst‐1 and cyclin DI, both of which are located in chromosome 11q13, was found in 9 cell lines. Without exception their amplification was simultaneous and the magnitudes were similar. Their amplification, but not their overexpression, was significantly correlated with poor prognosis in patients from whom the cell lines were established. While hst‐1‐gene expression was not detected, at least 1 of the genes analyzed was overexpressed in 20 cell lines vs. its expression in normal esophageal mucosal tissues. However, gene amplification was not necessarily accompanied by overexpression of the corresponding genes. Expression of the cyclin DI gene, which has been assumed to be a target gene for 11q13 amplification, was not detected in one particular cell line with amplification of 11q13. These results suggest that the amplification/overexpression of more than I oncogene is involved in the carcinogenic process of esophageal carcinoma and that c‐myc‐gene amplification is associated with a well‐differentiated subtype. There remains a possibility that key oncogenes other than cyclin DI are involved in 11q13 amplification.
UR - http://www.scopus.com/inward/record.url?scp=0027983696&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0027983696&partnerID=8YFLogxK
U2 - 10.1002/ijc.2910580224
DO - 10.1002/ijc.2910580224
M3 - Article
C2 - 7913084
AN - SCOPUS:0027983696
VL - 58
SP - 291
EP - 297
JO - International journal of cancer. Journal international du cancer
JF - International journal of cancer. Journal international du cancer
SN - 0020-7136
IS - 2
ER -