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Precancerous lesoins of the human esophagus: Multipliparameteric study of esophageal biopsies from a high‐risk populatiion in linxian, China
Author(s) -
Yang Kan,
Liu Yanhui,
Lipkin Martin,
Wang Guoqing,
Mou Dunxue,
Li Guangyi,
Li Juyao,
Li Ping
Publication year - 1992
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.240501132
Subject(s) - pathology , esophagus , dysplasia , hyperplasia , epithelium , basal (medicine) , histopathology , biology , immunohistochemistry , cell , carcinoma , medicine , anatomy , endocrinology , biochemistry , insulin
Abstract Histopathology, morphometry, tritiated thymidin incorporation and immunohistochemistry were studied in 221 esophageal biospies from subjects with cytologica hyperplasia in Linxian, China. A spectrum of 7 morphologic entities were found (1) normal/near normal (NN); (2) basal cell hyperplasia 0 (BHO); (3) simple hyperplasia (SH); (4) mixed basal and spinous cell hyperplasia (MBS); (5) basal cell hyperplasia 1 (BH1); (6) dysplasia (D); and (7) non‐profilerative lesion (NP). Forty percent of the biospies had combinations of histologic types. The thickness of the epithelium was increased in SH, MBS, and BH1, but not in BHO and NP Elongation of papiallae was frequent seen in SH, MBS, BH1, and D. Papillary bleeding was very prevalent in the esophageal specimens studied. A variety of cellular changes were found in peripapillary areas especially when bleeding occurred. [ 3 H]‐thymidine labeling index was dramatically increased in the entire epithelium in dysplasia, and also increased in cell layer 3 of MBS, BH1 and D. Blood group antigen Le Y and lectin WGA showed consistent positivity in cellular membranes of the squamous cells, and these changes ocuurred before gross morphologic alterations. These findings provide a hypothesis for the sequences of pathogenetic events leading to esophgeal carcinoma, and define each step with corresponding biomakers for cancer prevention studies. © 1992 Wiley‐Liss, Inc.