TY - JOUR
T1 - Changes in p53 and cyclin D1 protein levels and cell proliferation in different stages of human esophageal and gastric‐cardia carcinogenesis
AU - Wang, Li Dong
AU - Shi, Stephanie Tao
AU - Zhou, Qi
AU - Goldstein, Susan
AU - Hong, Jun‐Yan ‐Y
AU - Shao, Peter
AU - Qiu, Song‐Liang ‐L
AU - Yang, Chung S.
PY - 1994/11/15
Y1 - 1994/11/15
N2 - The objective of this study was to quantify the changes in p53 and cyclin DI protein levels in different stages of human esophageal and gastric cardia carcinogenesis in a high‐risk population in Henan, China. Immunoreactivity of p53, cyclin DI and proliferating‐cell nuclear antigen (PCNA) was observed in the cell nuclei of esophageal and gastric cardia biopsies. The number of p53‐immunostaining‐positive cells was low in normal epithelia, slightly increased in basal‐cell hyperplasia (BCH), markedly increased in dysplasia (DYS) (10‐fold), and further increased in squamous‐cell carcinoma (SCC) (40‐fold). This pattern of change was similar to that of cell proliferation as indicated by PCNA immunostaining. On the other hand, the number of cyclin DI‐immunostaining‐positive cells did not increase from BCH to DYS, although a slight increase from DYS to SCC was noted. In the gastric cardia, again, the pattern of change of p53‐positive cells in different stages of lesions paralleled the pattern of cell proliferation. The number of p53‐positive cells was very low, much lower than that of PCNA‐positive cells, in normal, chronic superficial gastritis (CSG) and chronic atrophic gastritis (CAG); therefore, the increase of p53‐positive cells from CAG to DYS was more dramatic (100‐fold). From DYS to adenocarcinoma (AC), the p53‐positive and the PCNA‐positive cells increased 4‐fold. On the other hand, the number of cyclin DI‐positive cells did not increase in pre‐cancerous lesions, but increased slightly in AC. This study demonstrates that p53 protein accumulation increased with the progression of pre‐cancerous lesions, especially in the genesis of dysplasia, both in the esophagus and in the gastric cardia. Our approach of quantitative immunohistochemistry sheds light on the mechanisms of genesis of esophageal and gastric‐cardia cancers, which frequently occur together in many highincidence areas. © 1994 Wiley‐Liss, Inc.
AB - The objective of this study was to quantify the changes in p53 and cyclin DI protein levels in different stages of human esophageal and gastric cardia carcinogenesis in a high‐risk population in Henan, China. Immunoreactivity of p53, cyclin DI and proliferating‐cell nuclear antigen (PCNA) was observed in the cell nuclei of esophageal and gastric cardia biopsies. The number of p53‐immunostaining‐positive cells was low in normal epithelia, slightly increased in basal‐cell hyperplasia (BCH), markedly increased in dysplasia (DYS) (10‐fold), and further increased in squamous‐cell carcinoma (SCC) (40‐fold). This pattern of change was similar to that of cell proliferation as indicated by PCNA immunostaining. On the other hand, the number of cyclin DI‐immunostaining‐positive cells did not increase from BCH to DYS, although a slight increase from DYS to SCC was noted. In the gastric cardia, again, the pattern of change of p53‐positive cells in different stages of lesions paralleled the pattern of cell proliferation. The number of p53‐positive cells was very low, much lower than that of PCNA‐positive cells, in normal, chronic superficial gastritis (CSG) and chronic atrophic gastritis (CAG); therefore, the increase of p53‐positive cells from CAG to DYS was more dramatic (100‐fold). From DYS to adenocarcinoma (AC), the p53‐positive and the PCNA‐positive cells increased 4‐fold. On the other hand, the number of cyclin DI‐positive cells did not increase in pre‐cancerous lesions, but increased slightly in AC. This study demonstrates that p53 protein accumulation increased with the progression of pre‐cancerous lesions, especially in the genesis of dysplasia, both in the esophagus and in the gastric cardia. Our approach of quantitative immunohistochemistry sheds light on the mechanisms of genesis of esophageal and gastric‐cardia cancers, which frequently occur together in many highincidence areas. © 1994 Wiley‐Liss, Inc.
UR - http://www.scopus.com/inward/record.url?scp=0028075502&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028075502&partnerID=8YFLogxK
U2 - https://doi.org/10.1002/ijc.2910590414
DO - https://doi.org/10.1002/ijc.2910590414
M3 - Article
C2 - 7960222
VL - 59
SP - 514
EP - 519
JO - International Journal of Cancer
JF - International Journal of Cancer
SN - 0020-7136
IS - 4
ER -