CORRELATION OF EPITHELIAL PROLIFERATION AND SQUAMOUS ESOPHAGEAL HISTOLOGY IN 1185 BIOPSIES FROM LINXIAN, CHINA

被引:4
作者
LIU, FS
DAWSEY, SM
WANG, GQ
RAO, M
LIPKIN, M
LEWIN, KJ
LI, JY
LI, B
TAYLOR, PR
机构
[1] NCI, DIV CANC PREVENT & CONTROL, CANC PREVENT STUDIES BRANCH, BETHESDA, MD 20892 USA
[2] CHINESE ACAD MED SCI, INST CANC, BEIJING, PEOPLES R CHINA
[3] MEM SLOAN KETTERING CANC CTR, NEW YORK, NY 10021 USA
[4] UNIV CALIF LOS ANGELES, CTR HLTH SCI, LOS ANGELES, CA USA
[5] CHINA CANC RES FDN, BEIJING, PEOPLES R CHINA
关键词
D O I
10.1002/ijc.2910550410
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Epithelial proliferation is an active area of research in gastrointestinal cancer, but only a few studies have examined the relationship of esophageal epithelial proliferation and squamous histologic findings in populations with high rates of squamous esophageal cancer. In order to study this correlation, tritiated thymidine labeling was performed on 1185 esophageal biopsies from 745 residents of Linxian, China, a county with some of the highest esophageal-cancer rates in the world. Total labeling index (TLI = total labeled cells/total cells counted) was used to measure the amount of proliferation, and the proportion of labeled cells found in cell layers 4 to 10 (labeled cell fraction 4 plus, LF4+ = labeled cells in layers 4-10/total labeled cells) was used to measure the vertical distribution of proliferation. Of the biopsies, 979 were histologically normal, 51 showed acanthosis, 35 showed esophagitis, 116 showed squamous dysplasia, and 6 showed invasive squamous cancer. The mean values of both proliferation variables, stratified by histologic diagnosis, showed the following relationships: normal = acanthosis < esophagitis = dysplasia < cancer. The ranges of proliferation values overlapped extensively in all biopsy categories, so that measuring proliferation could not substitute for histologic diagnosis. It remains to be seen whether proliferation values, histologic diagnoses, or some combination of these methods is most predictive of subsequent esophageal cancer. (C) 1993 Wiley-Liss, Inc.
引用
收藏
页码:577 / 579
页数:3
相关论文
共 13 条
[1]  
CRESPI M, 1979, LANCET, V2, P217
[2]   A GENETIC MODEL FOR COLORECTAL TUMORIGENESIS [J].
FEARON, ER ;
VOGELSTEIN, B .
CELL, 1990, 61 (05) :759-767
[3]  
Li J Y, 1982, Natl Cancer Inst Monogr, V62, P113
[4]  
LI JY, 1986, J NUTR GROWTH CANCER, V3, P199
[5]  
Li M H, 1980, Adv Cancer Res, V33, P173
[6]  
LIPKIN M, 1988, CANCER RES, V48, P235
[7]  
LIVSTONE EM, 1977, GASTROENTEROLOGY, V73, P1315
[8]  
MUNOZ N, 1982, LANCET, V1, P876
[9]  
MUNOZ N, 1985, INT J CANCER, V36, P187, DOI 10.1002/ijc.2910360210
[10]  
WANG LD, 1993, CANCER EPIDEM BIOMAR, V2, P71