Gastric Intestinal Metaplasia with Dysplasia-Like Atypia: A Morphological and Biologic Evaluation
Yuan Li, Xiaoyan Chang, Weixun Zhou, Yu Xiao, Jie Chen, Gregory Y Lauwers. Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China; Massachusetts General Hospital, Boston, MA
Background: Gastric intestinal metaplasia (IM) can be hyperproliferative and display cytoarchitectural atypia. These changes fall short of qualifying for dysplasia and have been generally classified as indefinite for dysplasia. Few studies have evaluated the prevalence and the morphologic and biologic characteristics of this variant of gastric IM.
Design: Out of an institutional cohort of biopsies with chronic atrophic gastritis and/or dysplasia obtained from ethnic Chinese, we categorized the cases as either 1) simple IM (SIM) with uniform glands, mature goblet cells, basally oriented nuclei and surface maturation; 2) IM with hyperplasia (IMH) showing limited architectural abnormalities, reduced number of goblet cells, slightly elongated and hyperchromatic nuclei and surface maturation; 3) IM with dysplasia-like atypia (IM-DLA) showing crowded glands varying in size and shape with mucin depletion, hyperchromatic nuclei, moderate pseudostratification and surface maturation; or 4) gastric dysplasia (GED). The relationship between the morphologic subgroups and various clinicopathological features, mucin immunophenotypes (gastric-, gastrointestinal-, intestinal-, and small intestinal-type) and biologic characteristics (p53, Ki-67 and AMACR) was evaluated.
Results: The final cohort consisted of 554 cases including 424 SIM, 93 IMH, 16 IM-DLA, and 21 GED cases. Notably, IM-DLA had a prevalence (3.8%) similar to GED (5.0%). Both of these lesions were similar in body/fundus distribution (12.5%), common association with surface erosion (18.8%), acute inflammation (62.5%) and paucity of goblet cells (68.8%). IM-DLA and GED also shared biologic similarities but with a lower frequency of AMACR expression (25% vs. 62%), p53 expression (6.3% vs. 47.6%) and increased Ki-67 index on surface/pit and isthmic zones in IM-DLA. However, intestinal and gastric immunophenotypes and ectopic superficial MUC6 expression were found exclusively in GED (p<0.001). Alternatively, SIM and IMH (individually or combined) statistically differed from IM-DLA and GED with regard to the various characteristics evaluated.
Conclusions: Gastric IM can be divided into 2 broad categories, one combining SIM and IMH, and the other IM-DLA. These variants of IM are readily defined by cytoarchitectural and biologic characteristics. Based on the similarities between GED and IM-DLA, we postulate that IM-DLA represents an early step in the gastric carcinogenic sequence.
Monday, March 19, 2012 1:00 PM
Poster Session II # 101, Monday Afternoon