Preinvasive Neoplasia in the Stomach: Diagnosis and Treatment
2007; Elsevier BV; Volume: 5; Issue: 9 Linguagem: Inglês
10.1016/j.cgh.2007.07.004
ISSN1542-7714
AutoresAmy Noffsinger, Irving Waxman,
Tópico(s)Metastasis and carcinoma case studies
ResumoThis article discusses the proper handling of biopsy samples from mucosal lesions taken from the stomach when there is a suspicion of a malignant process. In addition, the use of endoscopic mucosal resection for therapy and staging of gastric neoplasia is discussed. This article discusses the proper handling of biopsy samples from mucosal lesions taken from the stomach when there is a suspicion of a malignant process. In addition, the use of endoscopic mucosal resection for therapy and staging of gastric neoplasia is discussed. Gastric cancer is one of the most common cancers diagnosed worldwide, and it is the second most common cause of cancer deaths.1Parkin D.M. Global cancer statistics in the year 2000.Lancet Oncol. 2001; 2: 533-543Abstract Full Text Full Text PDF PubMed Scopus (2173) Google Scholar In 2002, 0.9 million new cases of gastric cancer were diagnosed, and 0.7 million people around the world died from the disease. There is a wide geographic variation in gastric cancer incidence, however, with eastern Asian countries such as Korea and Japan having the highest gastric cancer rates. In contrast, the incidence of gastric cancer is relatively low in much of Europe, North America, and Africa.2Ferlay J. Bray F. Pisani P. GLOBOCAN 2002: cancer incidence, mortality and prevalence worldwide IARC CancerBase no. 5, version 2.0. IARC Press, Lyon2004Google Scholar In many countries with high rates of gastric cancer, mass screening programs are in effect. In Japan, for example, the introduction of mass screening resulted in an increase in the proportion of cancers diagnosed at an early stage (mucosal or submucosal invasion) from 8% during the period from 1960 to 1964 to 50% in 1975 to 1979.3Nagata T. Ikeda M. Nakayama F. Changing state of gastric cancer in Japan—histologic perspective of the past 76 years.Am J Surg. 1983; 145: 226-233Abstract Full Text PDF PubMed Scopus (76) Google Scholar Currently, as many as 60% of gastric cancers in Japan are early lesions at the time of diagnosis.4Hisamichi S. Screening for gastric cancer.World J Surg. 1989; 13: 31-37Crossref PubMed Scopus (127) Google Scholar In countries such as the United States, however, where gastric cancer remains relatively uncommon, mass screening is not cost effective. As a result, targeted screening programs are used for patients deemed to be at high risk for developing the disease. High-risk groups include those with the premalignant lesions listed in Table 1. Screening also may be performed in patients with dyspeptic symptoms who are older than age 40.5Fielding J.W. Ellis D.J. Jones B.G. et al.Natural history of “early” gastric cancer: results of a 10-year regional survey.BMJ. 1980; 281: 965-967Crossref PubMed Scopus (90) Google Scholar The overall goal is detection of gastric precancerous lesions before they become invasive neoplasms or identification of gastric carcinomas at a stage when they still are curable.Table 1Diseases Associated With Premalignant Lesions of the StomachStatus after partial gastrectomyMénétrier’s diseaseFamilial adenomatous polyposisPeutz–Jeghers syndromeSporadic adenomatous polypsAtrophic gastritis with intestinal metaplasiaDysplasia Open table in a new tab We evaluated an 83-year-old man who was referred to the University of Chicago Medical Center for assessment of a flat gastric lesion found on EGD at an outside hospital. A biopsy specimen at the time of the original endoscopy showed at least intramucosal adenocarcinoma arising in a background of atrophic gastritis with intestinal metaplasia. The initial biopsy specimens contained essentially no submucosal tissue, and therefore, the depth of invasion of the lesion could not be determined with certainty by the pathologist. Subsequent endoscopic examination showed a flat, depressed, nonulcerated mass in the prepyloric region of the stomach. The lesion did not involve the entire circumference of the stomach. Endoscopic ultrasound showed a hypoechoic sessile mass with well-defined endosonographic borders. The lesion appeared to invade into the deep mucosa (layer 2). No abnormal-appearing lymph nodes were seen during endosonographic examination of the mediastinum and upper abdomen. Because the gastric mass appeared endosonographically to represent an intramucosal lesion, 30 mL of a solution of 1.25% Gonak (Akorn Inc, Decatur, IL), (hydroxypropyl methyl cellulose ophthalmic solution) with indigo carmine and saline was injected for a lift polypectomy. Endoscopic submucosal resection was performed successfully, and the deep resection site was closed with Resolution clips (Microvasive Endoscopy, Boston Scientific, Natick, MA). The specimen was recovered and submitted to the Surgical Pathology laboratory submucosal side down on filter paper for orientation. The specimen received in the Surgical Pathology laboratory consisted of a tan edematous but flat tissue fragment measuring 1.5 × 1.4 × 0.2 cm. The resection margin was inked and the specimen was sectioned serially and entirely submitted for histopathologic examination. Microscopically, the lesion represented an intramucosal adenocarcinoma without submucosal invasion. No angiolymphatic invasion was present, and the margins of resection were negative for neoplasia (Figure 1). The patient was discharged from the hospital on the following day with no complications. Considerable attention has been paid to the recognition and definition of premalignant gastric lesions. A precancerous condition is defined as a clinical state associated with a significantly increased risk of cancer. In contrast, a precancerous lesion represents a morphologically altered tissue in which cancer is more likely to occur than in its apparently normal counterpart. In many situations in which a precancerous condition exists there is also a demonstrable precancerous lesion. Thus, chronic atrophic gastritis represents a precancerous condition, and its association with epithelial dysplasia in an atrophic fundic mucosa constitutes a precancerous lesion that increases the risk for gastric cancer. Chronic atrophic gastritis, especially when accompanied by intestinal metaplasia, represents an adaptive response to long-standing chronic inflammation, and both lesions commonly precede and/or accompany the intestinal type of gastric carcinoma, particularly in high-incidence areas. The relationship of chronic gastritis and intestinal metaplasia to gastric cancer has been studied extensively and the evidence for a relationship derives from several sources. The prevalence of chronic atrophic gastritis closely correlates with the death rate from gastric carcinoma and, in follow-up studies, chronic atrophic gastritis has preceded the development of gastric malignancies.6Imai T. Kubo T. Watanabe H. Chronic gastritis in Japanese with reference to high incidence of gastric carcinoma.J Natl Cancer Inst. 1971; 47: 179-195PubMed Google Scholar, 7Siurala M. Varis K. Wioljasalo M. Studies of patients with atrophic gastritis: a 10–15 year follow-up.Scand J Gastroenterol. 1966; 1: 40-48PubMed Google Scholar The intestinal type of gastric cancer represents the end result of a series of mutations or cell transformations that begin 2 or more decades before a clinical diagnosis of cancer is established.8Correa P. Haenszel W. Cuello C. et al.A model for gastric cancer epidemiology.Lancet. 1975; 2: 58-60Abstract PubMed Scopus (906) Google Scholar The appearance of chronic gastritis represents an initial and necessary step in the process. Diverse types of chronic gastritis are associated with the subsequent development of cancer but the degree of cancer risk varies according to the type of gastritis present. Environmental chronic gastritis represents the most common gastric precancerous condition. However, autoimmune chronic gastritis also is associated statistically with the subsequent development of gastric cancer. In contrast, hypersecretory chronic gastritis is not associated commonly with cancer. In its early stages, gastritis appears as multiple small foci at the corpus-antrum junction. Each focus enlarges to cover a larger surface and eventually becomes confluent with neighboring foci, thereby involving larger areas of the antrum. The process also expands proximally into the gastric body, ultimately involving the fundus. These changes particularly affect the lesser curvature. If gastritis persists, gastric atrophy occurs followed by intestinal metaplasia. This begins the chain of progressive gastric mucosal lesions that eventually result in neoplasia. Gastric dysplasia may be either flat or polypoid (gastric adenoma), and may be very difficult to distinguish from regenerating gastric glands. True dysplasia, or intraepithelial neoplasia, usually is recognized by a combination of cytologic atypia, abnormal differentiation, and disturbed mucosal architecture. Areas of dysplasia are recognized by nuclear abnormalities including increased size, hyperchromasia, and an irregular shape. The pathologist always should scrutinize gastric biopsy specimens containing chronic atrophic gastritis and intestinal metaplasia for the presence of dysplastic changes. Most pathologists use a 2-tiered grading system in which gastric dysplasia is divided into low-grade and high-grade forms. Low-grade dysplasia is characterized by mild cytologic and architectural atypia (Figure 2). Abnormal cytologic features include the presence of enlarged, rounded, or ovoid vesicular nuclei with prominent nucleoli. Increasing dysplasia is accompanied by nuclear hyperchromasia, pleomorphism, anisocytosis, and decreased mucin secretion. Similar cytologic changes are seen in some examples of regenerative atypia. However, regenerative changes usually are accompanied by inflammation without significant abnormalities of architecture or differentiation. In high-grade dysplasia, normal nuclear polarity also is lost, and the cells appear disorganized and no longer line up along the basement membrane (Figure 2). Considerable interobserver variation exists in the diagnosis of gastric dysplasia. In 1 series, approximately one half of cases diagnosed as dysplasia by generalist pathologists were diagnosed as nonneoplastic (regenerative or reactive) by gastrointestinal pathologists.9Fertitta A.M. Comin U. Terruzzi V. et al.Clinical significance of gastric dysplasia: a multicenter follow-up study Gastrointestinal Endoscopic Pathology Study Group.Endoscopy. 1993; 25: 265-268Crossref PubMed Scopus (107) Google Scholar Not surprisingly, this variability is most pronounced when the diagnosis is low-grade dysplasia; much better agreement is reached on the diagnosis of high-grade dysplasia. Dysplasia is identifiable in up to 100% of early gastric cancers and in up to 80% of advanced cancers.10Oehlert W. Keller P. Henke M. et al.Gastric mucosal dysplasia: what is its clinical significance?.Front Gastrointest Res. 1979; 4: 173-182Crossref PubMed Google Scholar, 11Lewin K.J. Appleman H.D. Carcinoma of the stomach Tumors of the esophagus and stomach.in: Rosai J. Sobin L.H. Atlas of tumor pathology (3rd series). Armed Forces Institute of Pathology, Washington, DC1996: 245-330Google Scholar The presence of associated dysplasia in a smaller proportion of advanced cancers most likely is explained by the fact that larger neoplasms often overgrow adjacent precancerous lesions. The risk of progression of dysplasia to cancer is highest in patients with high-grade dysplasia, with 70% or more of these patients progressing on to the development of invasive carcinoma.9Fertitta A.M. Comin U. Terruzzi V. et al.Clinical significance of gastric dysplasia: a multicenter follow-up study Gastrointestinal Endoscopic Pathology Study Group.Endoscopy. 1993; 25: 265-268Crossref PubMed Scopus (107) Google Scholar, 12Lansdown M. Quirke P. Dixon M.F. et al.High-grade dysplasia of the gastric mucosa: a marker for gastric carcinoma.Gut. 1990; 31: 977-983Crossref PubMed Scopus (141) Google Scholar, 13Farinati F. Rugge M. Di Maro F. et al.Early and advanced gastric cancer in the follow-up of moderate and severe dysplasia patients A prospective study.Endoscopy. 1993; 25: 261-264Crossref PubMed Google Scholar, 14Saraga E.P. Gardiol D. Costa J. Gastric dysplasia A histological follow-up study.Am J Surg Pathol. 1987; 11: 788-796Crossref PubMed Scopus (107) Google Scholar, 15Rugge M. Farinati F. Baffa R. et al.Gastric epithelial dysplasia in the natural history of gastric cancer: a multicenter prospective follow-up study.Gastroenterology. 1994; 107: 1288-1296Abstract Full Text PDF PubMed Google Scholar Progression of low-grade dysplasia to higher-grade dysplasia or invasive carcinoma occurs at a lower rate (approximately 15%–25%), and the progression appears to be relatively slow.9Fertitta A.M. Comin U. Terruzzi V. et al.Clinical significance of gastric dysplasia: a multicenter follow-up study Gastrointestinal Endoscopic Pathology Study Group.Endoscopy. 1993; 25: 265-268Crossref PubMed Scopus (107) Google Scholar, 13Farinati F. Rugge M. Di Maro F. et al.Early and advanced gastric cancer in the follow-up of moderate and severe dysplasia patients A prospective study.Endoscopy. 1993; 25: 261-264Crossref PubMed Google Scholar, 15Rugge M. Farinati F. Baffa R. et al.Gastric epithelial dysplasia in the natural history of gastric cancer: a multicenter prospective follow-up study.Gastroenterology. 1994; 107: 1288-1296Abstract Full Text PDF PubMed Google Scholar As many as half of low-grade dysplasias reportedly remain stable or even regress, a fact that has suggested to some that the original diagnosis in many of these cases may have represented misinterpretation of reactive changes as low-grade dysplasia.12Lansdown M. Quirke P. Dixon M.F. et al.High-grade dysplasia of the gastric mucosa: a marker for gastric carcinoma.Gut. 1990; 31: 977-983Crossref PubMed Scopus (141) Google Scholar, 16Bearzi I. Brancorsini D. Santinelli A. et al.Gastric dysplasia: a ten-year follow-up study.Pathol Res Pract. 1994; 190: 61-68Crossref PubMed Scopus (63) Google Scholar Early gastric carcinoma is defined as a cancer that remains limited to the mucosa or to the mucosa and submucosa. The term early gastric carcinoma is not synonymous with intramucosal carcinoma, which infiltrates only the mucosa and does not invade the submucosa. It also is not synonymous with carcinoma in situ, a term that has been replaced by high-grade dysplasia. In countries with a high incidence of gastric cancer, refined fiberoptic endoscopy, combined with adequate cytologic and histologic sampling, formed the basis for large-scale screening programs for gastric cancer in asymptomatic patients and allowed the identification of a high percentage of early carcinomas. The proportion of early gastric cancers in patients in Japan is now greater than 50%.4Hisamichi S. Screening for gastric cancer.World J Surg. 1989; 13: 31-37Crossref PubMed Scopus (127) Google Scholar, 17Folli S. Dente M. Dell’Amore D. et al.Early gastric cancer: prognostic factors in 223 patients.Br J Surg. 1995; 82: 952-956Crossref PubMed Scopus (106) Google Scholar, 18Sue-Ling H.M. Martin I. Griffith J. et al.Early gastric cancer: 46 cases treated in one surgical department.Gut. 1992; 33: 1318-1322Crossref PubMed Scopus (113) Google Scholar, 19Everett S.M. Axon A.T. Early gastric cancer in Europe.Gut. 1997; 41: 142-150Crossref PubMed Scopus (249) Google Scholar In Western countries, the incidence of early gastric cancer is significantly lower, about 20% of gastric cancer cases.4Hisamichi S. Screening for gastric cancer.World J Surg. 1989; 13: 31-37Crossref PubMed Scopus (127) Google Scholar, 17Folli S. Dente M. Dell’Amore D. et al.Early gastric cancer: prognostic factors in 223 patients.Br J Surg. 1995; 82: 952-956Crossref PubMed Scopus (106) Google Scholar, 18Sue-Ling H.M. Martin I. Griffith J. et al.Early gastric cancer: 46 cases treated in one surgical department.Gut. 1992; 33: 1318-1322Crossref PubMed Scopus (113) Google Scholar, 19Everett S.M. Axon A.T. Early gastric cancer in Europe.Gut. 1997; 41: 142-150Crossref PubMed Scopus (249) Google Scholar Histologically, most early gastric cancers are well-differentiated, tubular, or papillary types with intestinal features; sometimes a pre-existing adenoma is recognizable. Flat early cancers tend to be poorly differentiated or signet-ring carcinomas of the diffuse type. Ulcerated cancers usually are either of the intestinal or the diffuse type. In most cases, endoscopic biopsy specimens permit a straightforward diagnosis of early gastric cancer, but occasionally problems arise. The most common of these include the following: (1) there are a small number of signet-ring cells within the lamina propria that can be missed easily; and (2) the distinction of high-grade dysplasia from intramucosal carcinoma often is difficult. In the case of signet-ring cell cancers, the use of cytokeratin or mucin stains may aid the pathologist in the identification of individual infiltrating cells (Figure 3). In addition, immunohistochemical staining for E-cadherin may show loss of expression of this protein in the neoplastic cells, whereas staining is retained in the surrounding nonneoplastic gastric epithelium (Figure 3). Intramucosal adenocarcinoma of the intestinal type is recognized when small glands bud into the lamina propria, or when individual cells invading the lamina propria are seen. Desmoplasia generally is not present and therefore should not be relied on as a feature of invasion. Generally speaking, multiple biopsy specimens, particularly from the edges of the lesion, and simultaneous cytologic brush sampling usually are adequate for diagnosis, even of minute (<5 mm in diameter) carcinomas. In addition, communication of an accurate and complete clinical history, including radiographic and endoscopic findings, can make the pathologist aware of the suspicion of a neoplastic process, and will assist him or her in evaluating a biopsy specimen for gastric neoplasia. At present, there are no established guidelines for the management of gastric dysplasia. Endoscopic follow-up evaluation usually is recommended when a diagnosis of low-grade dysplasia has been made, although this remains controversial.20Kapadia C.R. Gastric atrophy, metaplasia, and dysplasia: a clinical perspective.J Clin Gastroenterol. 2003; 36: S29-S36Crossref PubMed Scopus (110) Google Scholar A surveillance interval of 3–6 months at least during the first year is common,9Fertitta A.M. Comin U. Terruzzi V. et al.Clinical significance of gastric dysplasia: a multicenter follow-up study Gastrointestinal Endoscopic Pathology Study Group.Endoscopy. 1993; 25: 265-268Crossref PubMed Scopus (107) Google Scholar, 15Rugge M. Farinati F. Baffa R. et al.Gastric epithelial dysplasia in the natural history of gastric cancer: a multicenter prospective follow-up study.Gastroenterology. 1994; 107: 1288-1296Abstract Full Text PDF PubMed Google Scholar, 16Bearzi I. Brancorsini D. Santinelli A. et al.Gastric dysplasia: a ten-year follow-up study.Pathol Res Pract. 1994; 190: 61-68Crossref PubMed Scopus (63) Google Scholar, 21Farinati F. Rugge M. Di Mario F. et al.Early and advanced gastric cancer in the follow-up of moderate and severe gastric dysplasia patients A prospective study. I.G.G.E.D. Interdisciplinary Group on Gastric Epithelial Dysplasia.Endoscopy. 1993; 25: 261-264Crossref PubMed Scopus (86) Google Scholar, 22Di Gregorio C. Morandi P. Fante R. et al.Gastric dysplasia A follow-up study.Am J Gastroenterol. 1993; 88: 1714-1719PubMed Google Scholar but it is unclear how long surveillance should continue, especially when subsequent surveillance biopsy specimens are negative for dysplasia, as is commonly the case. At the time of surveillance endoscopy, multiple biopsy specimens should be taken throughout the stomach and placed in separate specimen containers for each location sampled. In this way, it is possible to determine whether any neoplastic lesions that are detected are localized or distributed diffusely throughout the stomach. This is important because localized lesions may be amenable to endoscopic mucosal resection (EMR), whereas multifocal lesions may require surgical resection, especially if the subsequently identified dysplasia is high grade. Because of its close association with adenocarcinoma, surgical resection previously was suggested in all cases after a diagnosis of high-grade dysplasia. Currently, however, endoscopic ultrasonography and EMR offer a nonsurgical, potentially curative alternative for the treatment of these lesions.15Rugge M. Farinati F. Baffa R. et al.Gastric epithelial dysplasia in the natural history of gastric cancer: a multicenter prospective follow-up study.Gastroenterology. 1994; 107: 1288-1296Abstract Full Text PDF PubMed Google Scholar, 23Ono H. Kondo H. Gotoda T. et al.Endoscopic mucosal resection for treatment of early gastric cancer.Gut. 2001; 48: 225-229Crossref PubMed Scopus (1399) Google Scholar, 24Hiki Y. Shimao H. Mieno H. et al.Modified treatment of early gastric cancer: evaluation of endoscopic treatment of early gastric cancers with respect to treatment indication groups.World J Surg. 1995; 19: 517-522Crossref PubMed Scopus (74) Google Scholar, 25Takeshita K. Tani M. Inoue H. et al.Endoscopic treatment of early esophageal or gastric cancer.Gut. 1997; 40: 123-127PubMed Google Scholar EMR also may be used in the treatment of patients with intramucosal adenocarcinomas of the stomach. Lesions confined to the mucosa are associated with a low risk of lymph node metastasis (0%–3%), and are therefore amenable to EMR.26Sano T. Kobori O. Muto T. Lymph node metastasis from early gastric cancer: endoscopic resection of tumour.Br J Surg. 1992; 79: 241-244Crossref PubMed Scopus (383) Google Scholar, 27Yamao T. Shirao K. Ono H. et al.Risk factors for lymph node metastasis from intramucosal gastric carcinoma.Cancer. 1996; 77: 602-606Crossref PubMed Scopus (287) Google Scholar Recent studies have suggested that at least for small lesions (<1.5 to 2 cm) that are not poorly differentiated or ulcerated, EMR can be curative.27Yamao T. Shirao K. Ono H. et al.Risk factors for lymph node metastasis from intramucosal gastric carcinoma.Cancer. 1996; 77: 602-606Crossref PubMed Scopus (287) Google Scholar, 28Miyata M. Yokoyama Y. Okoyama N. et al.What are the appropriate indications for endoscopic mucosal resection for early gastric cancer? Analysis of 256 endoscopically resected lesions.Endoscopy. 2000; 32: 773-778Crossref PubMed Scopus (66) Google Scholar, 29Gotoda K. Yanagisawa A. Sasako M. et al.Incidence of lymph node metastasis from early gastric cancer The estimation using a large number of cases in two large centers.Gastric Cancer. 2000; 3: 219-225Crossref PubMed Scopus (1522) Google Scholar It also may be possible to endoscopically resect poorly differentiated intramucosal carcinomas if they are less than 1 cm in size and show no evidence of angiolymphatic invasion on pathologic examination.30Abe N. Watanabe T. Sugiyama M. et al.Endoscopic treatment or surgery for undifferentiated early gastric cancer?.Am J Surg. 2004; 188: 181-184Abstract Full Text Full Text PDF PubMed Scopus (79) Google Scholar To determine the risk for lymph node metastases, and the need for surgical resection, the depth of invasion and the presence of vascular or lymphatic invasion should be evaluated in all EMR specimens. In fact, EMR is used increasingly as the most accurate nonsurgical staging procedure on which further management can be based.31Tada M. Endoscopic mucosal resection of the stomach: initial description.Gastrointest Endosc Clin N Am. 2001; 11: 499-510PubMed Google Scholar, 32Larghi A. Lightdale C.J. Memeo L. et al.EUS followed by EMR for staging of high-grade dysplasia and early cancer in Barrett’s esophagus.Gastrointest Endosc. 2005; 62: 16-23Abstract Full Text Full Text PDF PubMed Scopus (189) Google Scholar, 33Hull M.J. Mino-Kenudson M. Nishioka N.S. et al.Endoscopic mucosal resection: an improved diagnostic procedure for early gastroesophageal epithelial neoplasms.Am J Surg Pathol. 2006; 30: 114-118Crossref PubMed Scopus (123) Google Scholar The ability to predict the risk of lymph node metastases requires proper preparation and careful pathologic examination of the resected specimen. Immediately after resection, EMR specimens should be flattened and pinned at their periphery with thin needles into a supportive backing such as a corkboard or a wax block before immersion into fixative. Serial sections at 2-mm intervals then should be obtained for histopathologic examination. To aid the clinical decision-making process, it is important that the pathologist’s report contain a detailed description of the location of the lesion (taken from the endoscopy report), size, type, and grading of the neoplasia, exact depth of tumor infiltration, presence of ulceration, neoplastic involvement of the lateral and deep margins, and invasion of lymphatics and vessels.34Vieth M. Stolte M. Pathology of early upper GI cancers.Best Pract Res Clin Gastroenterol. 2005; 19: 857-869Abstract Full Text Full Text PDF PubMed Scopus (75) Google Scholar, 35Soetikno R. Kaltenbach T. Yen R. et al.Endoscopic mucosal resection for early cancers of the upper gastrointestinal tract.J Clin Oncol. 2005; 23: 4490-4498Crossref PubMed Scopus (495) Google Scholar Despite the increased levels of diagnostic accuracy achievable by analysis of EMR specimens, conventional EMR techniques are limited in their capability of achieving en bloc resection, in particular for lesions greater than 2 cm in size.36Inoue H. Takeshita K. Hori H. et al.Endoscopic mucosal resection with a capfitted panendoscope for esophagus, stomach, and colon mucosal lesions.Gastrointest Endosc. 1993; 39: 58-62Abstract Full Text PDF PubMed Scopus (541) Google Scholar, 37Kojima T. Parra-Blanco A. Takahashi H. et al.Outcome of endoscopic mucosal resection for early gastric cancer: review of the Japanese literature.Gastrointest Endosc. 1998; 48: 550-554Abstract Full Text Full Text PDF PubMed Google Scholar, 38Inoue H. Tani M. Nagai K. et al.Treatment of esophageal and gastric tumors.Endoscopy. 1999; 31: 47-55Crossref PubMed Scopus (124) Google Scholar Such lesions often must be removed piecemeal, a factor that makes pathologic evaluation of resection margins difficult. In addition, higher rates of local tumor recurrence have been reported with piecemeal EMR than with en bloc resection.23Ono H. Kondo H. Gotoda T. et al.Endoscopic mucosal resection for treatment of early gastric cancer.Gut. 2001; 48: 225-229Crossref PubMed Scopus (1399) Google Scholar, 39Iishi H. Tatsuta M. Iseki K. et al.Endoscopic piecemeal resection with submucosal saline injection of large sessile colorectal polyps.Gastrointest Endosc. 2000; 51: 697-700Abstract Full Text Full Text PDF PubMed Scopus (144) Google Scholar, 40Katada C. Muto M. Manabe T. et al.Local recurrence of squamous-cell carcinoma of the esophagus after EMR.Gastrointest Endosc. 2005; 61: 219-225Abstract Full Text Full Text PDF PubMed Scopus (129) Google Scholar, 41Tamura S. Nakajo K. Yokoyama Y. et al.Evaluation of endoscopic mucosal resection for laterally spreading rectal tumors.Endoscopy. 2004; 36: 306-312Crossref PubMed Scopus (75) Google Scholar This led the Japanese Gastric Cancer Association to promote guidelines emphasizing that endoscopic treatment of early gastric cancer should be applied only to lesions whose size and location make them resectable in a single specimen.42Japanese Gastric Cancer AssociationGuidelines for gastric cancer treatment. Kanehara-Shuppan, Tokyo2001Google Scholar Because intramucosal adenocarcinoma is associated frequently with synchronous lesions and metachronous cancers can occur after EMR, an endoscopic follow-up program is very important. Two studies have shown that annual endoscopic examination allowing early diagnosis and endoscopic treatment of synchronous and metachronous lesions can lead to preservation of the whole stomach in most patients with early gastric cancer who have undergone successful EMR.43Nasu J. Doi T. Endo H. et al.Characteristics of metachronous multiple early gastric cancers after endoscopic mucosal resection.Endoscopy. 2005; 37: 990-993Crossref PubMed Scopus (135) Google Scholar, 44Nakajima T. Oda I. Gotoda T. et al.Metachronous gastric cancers after endoscopic resection: how effective is annual endoscopic surveillance?.Gastric Cancer. 2006; 9: 93-98Crossref PubMed Scopus (180) Google Scholar An algorithm for the treatment of patients with gastric dysplasia and early gastric cancer is shown in Figure 4. EMR provides an exciting new alternative for minimally invasive treatment of superficial gastrointestinal malignancies. An increasing body of evidence suggests that this technique can be performed safely and has comparable outcomes with surgery with less morbidity and better quality of life because of its tissue-sparing nature when compared with conventional surgery. Close cooperation and communication between the endoscopist and the pathologist is required for proper staging and treatment of such patients.
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