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What Is Dysplasia in the Gastrointestinal Tract?

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What Is Dysplasia in the Gastrointestinal Tract? What Is Dysplasia in the Gastrointestinal Tract? Henry D. Appelman, MD c Dysplasia in the gastrointestinal tract is considered both the skin and those in the salivary gland, the most prom- a carcinoma precursor and a marker of high cancer risk inent of which is the pleomorphic adenoma. These tumors for the site at which it is found. Dysplasia is de®ned as are composed of mature epithelium, and the risk of cancer unequivocally neoplastic epithelium, yet the speci®c cri- occurring within them is minute. It was no wonder that teria for making that determination are imperfectly de- the same name, adenoma, was used for polypoid epithelial ®ned. The current criteria actually include a mix of archi- proliferations, mainly in the colon, that were considered tectural and cytologic features, all of which occur in dif- neoplastic but not malignant. However, it was not known ferent intensities in different epithelia that are given the then that the things called adenomas in noncolonic sites same diagnosis. Gastrointestinal dysplasias are divided into were composed of mature epithelium, whereas the epi- 2 grades, but there are problem areas in diagnosis at the thelium in the colonic lesions of the same name was most- lower end where low-grade dysplasias overlap with regen- ly immature or at least less mature. In addition, at the time erating epithelia and in the middle where low- and high- of this naming, the concept of dysplasia as a cancer pre- grade dysplasias overlap. The diagnosis of dysplasia is too cursor was not well established, and the fact that the ep- subjective with less than optimal reproducibility to be as ithelium contained in those colonic adenomas was the useful a marker as needed. Pathologists need a dysplasia common colonic cancer precursor and identical to what stain or a whole set of new markers of high cancer risk, we now call dysplasia was not appreciated. Adenomas of presumably molecular and/or genetic, that are not depen- the gut are dysplasias and should be called by the dys- dent on pathologists' diagnoses of dysplasia and their in- plasia name. However, the term adenoma for noninvasive herent subjectivity. gut neoplasms is so much a part of our jargon that it will (Arch Pathol Lab Med. 2005;129:170±173) take an act of Congress or a natural catastrophe to get rid of it. e have identi®ed several models in the gastrointes- The answer to the second question, just what is this tinal tract in which there are postulated interme- dysplasia thing, is more complex and is the major subject W of this discussion. To be perfectly honest, the answer is diates between normal mucosa and invasive adenocarci- 1,2 noma. The most common of these models is typical or elusive and may not even be obtainable. Certainly, many ordinary colorectal carcinoma in which the intermediate people have tried to tell us what dysplasia is; there is a stage was given the name adenoma. Other such models are huge body of literature devoted to discussing and describ- adenocarcinomas that arise in the esophagus in Barrett ing dysplasia in various parts of the gut, and every text- mucosa, in the stomach in atrophic gastritis, and in the book of gastrointestinal pathology devotes plenty of space colon and rectum in chronic in¯ammatory bowel diseases, to it. There are so many references to dysplasia, that I have 3±9 mainly ulcerative colitis. In these cancer situations, the in- limited the reference list here to only a few examples. termediate stages, which look very much like histologic Dysplasia was de®ned as unequivocally neoplastic epithe- adenomas, are not called adenoma but instead are called lium by a group of supposedly experienced gastrointes- dysplasias. Why are there 2 different names for such his- tinal pathologists who were studying a large number of tologically similar adenocarcinoma intermediates, and just epithelial changes associated with chronic colitis, mostly 10 what is this dysplasia thing anyway? ulcerative colitis. The results of that study, copiously il- The answer to the ®rst question is the easiest. The term lustrated, were published in 1983; by now, it is old stuff. adenoma had been used for benign nonsquamous epithelial The de®nition they provided sounds fabulous, but exactly neoplasms, such as those with adnexal differentiation in how do we know what is unequivocally neoplastic? This decision is made by pathologists. Those supposedly ex- perienced gastrointestinal pathologists never said who Accepted for publication October 7, 2004. was responsible for making the critical decisions in spe- From the Department of Pathology, University Hospitals, Ann Arbor, Mich. ci®c cases as to what changes constituted unequivocally Presented at a pathology symposium held in conjunction with the neoplastic epithelium. How did those or any other pa- 7th World Congress of the International Organization for Specialized thologists learn how to make that decision? They were Studies on Diseases of the Esophagus, UNESCO Headquarters, Paris, able to make the decision because of several factors. The France, September 3, 2003. most important factor is their training. Perhaps someone The author has no relevant ®nancial interest in the products or com- older and wiser taught them the truth during their resi- panies described in this article. Reprints: Henry D. Appelman, MD, Department of Pathology, Uni- dencies, and maybe they took postgraduate courses from versity Hospitals, 1500 E Medical Center Dr, Room 2G332, Ann Arbor, alleged experts or sent cases to such experts. After all, the MI 48109-0054 (e-mail: [email protected]). reason we have experts is to teach us stuff, to give courses, 170 Arch Pathol Lab MedÐVol 129, February 2005 Dysplasia in the Gastrointestinal TractÐAppelman to act as consultants, and to write papers such as this one. a sequence that begins with native epithelium altered by Otherwise, why would we need them? Second, personal a combination of genetic and environmental factors. We experience plays a role, including clinical follow-up, which preach that this in turn leads to the development of ®rst gave these pathologists information as to what happened low-grade dysplasia, which then gives rise to high-grade to people they labeled as having this unequivocally neo- dysplasia and ®nally to invasive carcinoma. Perhaps much plastic epithelium. A third factor, which is not subject to of this supposition is based on the fact that epithelia di- debate, is the issue of guesswork, meaning that we all agnosed as low-grade dysplasia at a particular site are less make diagnostic guesses as best we can about many likely to be accompanied by invasive carcinoma than are things with which we are either unfamiliar or have limited epithelia diagnosed as high grade. Furthermore, when familiarity, and we offer these guesses as true diagnoses. low-grade dysplasia is found, the future risk of developing The next logical question is, how do we know whether invasive carcinoma at the speci®c site is less than that for this training, experience, and diagnostic guesswork are high-grade dysplasia, and it takes longer for carcinomas applicable to the particular problem? The answer is, we to develop. However, there is virtually no information on don't! As a result, all surgical pathologists who have var- what happens over time to a speci®c focus of low-grade iable training and variable experience are given the re- or high-grade dysplasia. Thus, dysplasias are de®nitely sponsibility of making determinations, and they have risk indicators for carcinoma, but there is little proof that done the best they can with little help because there are they are precursors. no clear sets of diagnostic criteria for each change they see Pathologists recognize many histologic alterations that in biopsies, even in the publication that summarized the are considered dysplastic changes. In the ®gures present- analyses of that distinguished group of supposedly ex- ed here, Barrett mucosa is used as a model. The alterations perienced gastrointestinal pathologists. Therefore, the def- are both architectural and cytologic. The architectural inition of dysplasia must include the fact that it is the in- changes involve differences from normal structure, such vention of pathologists, and it is both our responsibility as clustering and crowding of tubules, an exaggerated vil- and our fault. One of the most truthful de®nitions of dys- lous surface pattern, or the appearance of bridges of cells plasia comes from one of my colleagues: ``dysplasia is like that cross lumens. This last feature results in the classic pornography; I know it when I see it'' (J. K. Greenson, cribriform pattern of growth, a form of architectural com- MD, Professor of Pathology, University of Michigan, oral plexity. Other architectural changes involve the relation of communication, July 2003). the cells and their nuclei to other cells and are recognized Although the original dysplasia de®nitions and illustra- as nuclear and cellular strati®cation (Figures 1 through 4). tions were based on changes associated with in¯amma- The cytologic features are more complex and involved tory bowel diseases, mainly ulcerative colitis, these de®- both cytoplasm and nuclei. The cytoplasmic features most- nitions have been applied to other settings, such as colonic ly involve loss of maturation or specialization, such as de- adenomas, Barrett mucosa, and atrophic gastritis, but the crease in or loss of mucus content. The nuclear changes carcinomas and their intermediates evolve in remarkably include enlargement with increase in the ratio of nucleus different settings. Colonic adenomas arise in a background to cytoplasm, pleomorphism (ie, variation in size and of histologically normal, although presumably genetically shape), hyperchromatism (ie, increase in nucleic acid con- altered, colorectal mucosa. Barrett esophagus is a meta- tent causing the nuclei to stain more darkly than normal), plasia in which normal squamous mucosa in the lower and increase in the number of mitotic ®gures and unusual esophagus is replaced by columnar mucosa, as a result or strange looking mitoses (Figures 1 through 8).
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