Pyloric Gland Adenoma Research Articles

1928 A Rare Case of Hematemesis Due to a Large Gastric Pyloric Gland Adenoma

INTRODUCTION: Accounting for less than 3% of all gastric polyps, pyloric gland adenomas (PGAs) are rare tumors that usually arise from the stomach or, less commonly, the esophagus, duodenum, pancreas, or gallbladder. PGAs rarely cause symptoms and hematemesis as the presenting symptom has not been previously described in the literature. We present a rare case of hematemesis secondary to a large gastric PGA. CASE DESCRIPTION/METHODS: A 94 year-old female with a history of hypothyroidism and occasional nonsteroidal anti-inflammatory drug-use presented with hematemesis and hematochezia. She complained of acute-onset nausea, vomiting and diarrhea. Patient was hemodynamically stable at the time of presentation. Admission laboratory studies were significant for a hemoglobin of 7.2 mg/dl compared to 11.4 mg/dl two weeks prior. An esophagogastroduodenoscopy (EGD) was performed and revealed a 4 cm polyp-appearing mass with a short stalk in the mid-greater curvature of the body of the stomach. The tissue was friable and spontaneously bled with minimal friction from the snare, thus likely the etiology for the patient’s symptoms. The polyp was removed in piecemeal fashion using hot snare. Submucosal epinephrine was injected and four DuraClips were deployed over the polypectomy site. The patient declined to undergo a colonoscopy. Following her EGD, patient did not exhibit any additional signs or symptoms of continued bleeding and was discharged home in good condition. Pathology revealed pyloric gland adenoma with high-grade dysplasia. DISCUSSION: This case emphasizes the need for increased awareness regarding the presence of PGAs. These lesions have been shown to arise in chronically damaged mucosa and were associated with autoimmune gastritis in 33.9% of patients, active Helicobacter pylori-associated gastritis in 30.2% of patients, and normal gastric mucosa in only 3.8% of patients. Patients are usually elderly females with an average age of 75 years; though signs and symptoms are variable, laboratory evaluation frequently reveals anemia. This diagnosis is rare but the malignant potential was reported between 12 to 30% of cases in two large studies making improved classification and management necessary.

Early adenocarcinoma colliding with a pyloric gland adenoma in the gastric cardia

Early adenocarcinoma colliding with a pyloric gland adenoma in the gastric cardia

Endoscopic and histologic features associated with gastric cancer in familial adenomatous polyposis

Gastric cancer (GC) is a newly described cancer risk in Western patients with familial adenomatous polyposis (FAP). Little is known about clinical, endoscopic, and pathologic features associated with FAP-related GC. We compared these features in FAP patients with and without GC. FAP patients were identified through the David G. Jagelman Inherited Colorectal Cancer Registries Cologene database. FAP patients with GC and randomly selected FAP patients without GC who had undergone at least 2 EGDs were analyzed. Demographic, clinical, endoscopic, and pathologic features were compared. Ten FAP patients with GC were identified, and 40 age-matched FAP control subjects were selected. No demographic differences were noted between patients and control subjects. All GC cases arose in the proximal stomach among gastric polyposis, with only 2 endoscopically visible. The prevalence of gastric polyposis was similar (100% vs 93%). Endoscopic features associated with GC included a carpeting of gastric polyps (100% vs 22.5%), solitary polyps >20mm (100% vs 0%), and a polypoid mound of polyps (80% vs 0%; all P< .001). GC patients had a higher prevalence of gastric adenomas (30% vs 5%, P= .048) and polyps with high-grade dysplasia, including fundic gland polyps (50% vs 10%, P= .01) and pyloric gland adenomas (20% vs 0%, P= .037). We identified endoscopic features and advanced pathology present in the stomachs of Western patients with FAP who developed GC. Upper GI surveillance in FAP should include the stomach and awareness of features associated with GC. Optimal approaches to treatment of gastric polyposis and methods of identification of early GC precursors in FAP are needed.

Pyloric Gland Adenoma of Gallbladder: A Review of Diagnosis and Management.

Neoplastic polypoid mucosal lesions of the gallbladder are increasingly being reported in cholecystectomy specimens. However, due to the absence of unified terminology and reporting criteria, the body of scientific evidence on their classification, prognosis, and management is scarce and sometimes controversial. While they have different histomorphologic features (gastric foveolar, gastric pyloric gland, biliary, and intestinal), a significant immunohistochemical overlap exists which highlights their mixed cell lineage with a dominant cell type in each, establishing the subcategory. Because of many shared attributes, intracholecystic papillary-tubular neoplasm (ICPN) has been introduced as an umbrella terminology. ICPNs of the pyloric subtype are lesions larger than 1 cm, as most of the smaller ones are clinically insignificant and represent polypoid hyperplasia rather than a true neoplasm. In this review, we will focus on the pyloric gland adenomas as the most frequent histologic subtype of ICPNs.

Pyloric Gland Adenoma: Uncommon or Unrecognized?

Gastric pyloric gland adenomas (PGAs) are rare epithelial polyps that are found more commonly in autoimmune atrophic gastritis and familial adenomatous polyposis (FAP). PGA are clinically significant because they are neoplasms with malignant potential rather than a hyperplasia of metaplastic glands. We report a case of invasive adenocarcinoma arising from PGA with high grade dysplasia in a patient without history of pernicious anemia or FAP. An 80 year old female with a history of intermittent episodes of severe fecal urgency underwent CAT scan of the abdomen and pelvis for evaluation of possible GI tumors, which revealed polypoid irregular mass in the cardia measuring 3.6 x 3.4 cm. Subsequently, EGD confirmed the presence of 3cm circumferential polypoid mass at the cardia. Biopsy of the mass revealed pyloric gland adenoma with high grade dysplasia. Esophago-gastrectomy was performed and the final pathology results demonstrated well to moderately differentiated invasive adenocarcinoma, arising in low and high grade dysplasia, invading mucosa. Immunostains showed intact expression of mismatch repair proteins (MLH1, MSH2, MSH6 and PMS2) on tumor cells. Atrophic gastritis with intestinal metaplasia negative for H pylori was present. Tumor stage (AJCC 20010): pT1aN0 Gastric PGA have been shown to arise in chronically damaged mucosa. PGA was first mentioned in the 1990 WHO classification and was not fully described until 2003 by German investigator Vieth et al reported 90 such lesions encountered in the stomach, duodenum, bile duct, and gallbladder. This neoplasm has not been well recognized as a distinct entity in the US literature, until Chen ZM et al., reported the largest US series of 41 PGA in 2009. The greatest diagnostic challenge with PGAs is distinguishing them from foveolar-type adenomas. PGAs are probably more common than the literature suggests, have a characteristic histologic appearance, and have the capacity to evolve into infiltrating adenocarcinomas. In these two largest series, gastric PGAs have frequent association with adenocarcinoma, ranging from 12% to 30% of cases.2645_A Figure 1. Endoscopic image2645_B Figure 2. Intraoperative image2645_C Figure 3. HistologyWe present this case of invasive adenocarcinoma arising from pyloric gland adenoma with high grade dysplasia in a patient with atrophic gastritis. PGA were recognized years ago by European and Japanese pathologist whereas North American pathologists learned to diagnose them more recently, therefore these clinically significant lesions may be underrecognized and underreported.

Pyloric Gland Adenomas: Histologically Distinct yet Phenotypically Diverse Neoplasms of the GI Tract

Pyloric Gland Adenomas: Histologically Distinct yet Phenotypically Diverse Neoplasms of the GI Tract

Pyloric Gland Adenoma (PGA) of the Gallbladder: A Unique and Distinct Tumor from PGAs of the Stomach, Duodenum, and Pancreas.

Twenty-four surgically resected, gallbladder pyloric gland adenomas (GB-PGAs) were examined and their features were compared with the reported features of stomach, duodenum, and pancreatic PGAs to better understand GB-PGAs. Clinical information on background gallbladder lesions and histologic data, including tumor grade, existence of squamoid morules, intratumoral cholesterosis, and intracytoplasmic mucins were collected. Immunohistochemical staining for MUC2, MUC5AC, MUC6, CDX2, pepsinogen I, p53, and MIB-1/nuclear β-catenin were evaluated. Targeted mutational analyses of KRAS exon2, GNAS exon 7, and CTNNB1 exon 3 were conducted. We found that 29.2% of the GB-PGAs were histologically high-grade dysplasias/carcinomas; 70.8% were low grade; and 20.8% and 33.3% contained squamoid morules and intratumoral cholesterosis, respectively. In addition, 45.8% and 54.2% of GB-PGAs were mucin-rich and mucin-poor types, respectively. Immunohistochemically, MUC6 was diffusely positive in all GB-PGAs; MUC2, MUC5AC, and CDX2 were only focally positive, and no pepsinogen-I positive cells were observed. Nuclear β-catenin accumulation was observed in all cases; however, the ratio varied among cases. Mucin-poor types were significantly associated with high histologic grade dysplasias/carcinomas and high nuclear β-catenin labeling indices. Mutational analyses identified CTNNB1 mutations in 100% of GB-PGAs (21/21), KRAS in 4.2% (1/23), and GNAS in 0% (0/22). The present study clarified the unique histologic features, phenotypic differentiation, and molecular statuses frequently associated with GB-PGAs. Altogether, our data suggest that tumorigenesis of GB-PGA is distinct from that of stomach, duodenum, and pancreatic PGAs.

Heterotopic tissue in the gastrointestinal tract

Heterotopia of the gastrointestinal tract is acommon finding. This is due to the complex embryogenesis and the relative ease to detect heterotopic tissue during endoscopy. The reason for biopsy is mostly to rule out neoplasms or to define specific causes of inflammation. Heterotopic tissue can occur in any location of the gastrointestinal tract. The most frequent are gastric heterotopia, pancreatic heterotopia, and heterotopia of Brunner's gland. On rare occasions, heterotopic tissue of salivary gland type as well as heterotopias of apocrine glands, thyroid, and prostatic tissue have been described. The most frequently involved organs are the small intestine, in particular the duodenum, the esophagus, and the stomach. Heterotopia of the large bowel occurs exclusively in the rectum. Most heterotopias do not cause symptoms and are easily diagnosed by biopsy and histology. However, depending on location, size, and the kind of underlying heterotopic tissue, they may cause significant complications, such as inflammation, ulceration and perforation, obstruction, intussusception, and severe life-threatening bleeding. Another rare but significant complication is neoplasia. Gastric heterotopias may give rise to pyloric gland adenomas within the bowel or rarely adenocarcinomas of the esophagus. Pancreatic heterotopia can be complicated by ductal type pancreatic adenocarcinomas, by acinus cell carcinomas, by intraductal papillary mucinous neoplasias, and also by endocrine tumors. The present paper summarizes our current knowledge about heterotopias in atopographic clinico-pathological manner.

The outlet patch: gastric heterotopia of the colorectum and anus.

Gastric heterotopia (GH) has been described throughout the gastrointestinal tract. However, the colorectal region is an extremely rare location for it. We describe the clinicopathological features of GH of the colon, rectum and anus. We identified 33 cases in 20 males and 13 females (median age=54years; range=4months-73years). Sites included the rectum (n=26), anus (n=4), ileocaecal junction (n=1), ascending colon (n=1) and descending colon (n=1). Presenting symptoms (n=27) included haematochezia (41%) and altered bowel habits (4%); 15 patients (55%) were asymptomatic. On colonoscopy (n=31), all appeared as solitary lesions (median size=6.5mm, range=2-55mm), either as polyps (61%), raised erythematous patches (23%), an ulcer (10%), within a rectal diverticulum (3%) or a haemorrhoid (3%). Patients were managed by polypectomy. One with an associated carcinoma in the area of GH underwent resection. No morbidity related to GH itself was reported following excision. Histologically, heterotopic gastric mucosa was oxyntic (85%), mixed oxyntic and non-oxyntic (12%) and not specified (3%) types. In five patients a pyloric gland adenoma (PGA) arose from heterotopic gastric mucosa, two of which contained a focus of invasive adenocarcinoma. One case had associated surface foveolar-type low-grade dysplasia. Another had associated adenocarcinoma arising from the heterotopic mucosa. One example harboured Helicobacter pylori organisms. We highlight the features of GH in the distal GIT - the 'outlet patch'. Association with PGA, surface dysplasia and adenocarcinoma suggests thatlower tract GH can undergo neoplastic transformation.

Reduced αGlcNAc glycosylation on gastric gland mucin is a biomarker of malignant potential for gastric cancer, Barrett's adenocarcinoma, and pancreatic cancer.

Gastric gland mucin secreted from pyloric gland cells, mucous neck cells, and cardiac gland cells of the gastric mucosa harbors unique O-glycans carrying terminal α1,4-linked N-acetylglucosamine residues (αGlcNAc), which are primarily attached to the scaffold mucin core protein MUC6. αGlcNAc acts as an antibiotic against Helicobacter pylori (H. pylori), a microbe causing gastric cancer. In addition, mice deficient in A4gnt, which encodes the enzyme α1,4-N-acetylglucosaminyltransferase (α4GnT) that catalyzes αGlcNAc biosynthesis, spontaneously develop gastric differentiated-type adenocarcinoma, even if not infected by H. pylori. Thus, αGlcNAc prevents gastric cancer as both an antibiotic and a tumor suppressor (Nakayama in Acta Histochem Cytochem 47:1-9, 2014b). Indeed, in humans αGlcNAc loss on MUC6 in differentiated-type adenocarcinoma is closely associated with poor patient prognosis (Shiratsu et al. in Cancer Sci 105:126-133, 2014). Recently, we reported reduced αGlcNAc expression on MUC6 in both pyloric gland adenoma of the stomach and chronic atrophic gastritis, in Barrett's esophagus, and in pancreatic intraductal papillary-mucinous neoplasm (IPMN)/pancreatic intraepithelial neoplasia (PanIN), all potentially premalignant conditions. This review discusses whether relatively reduced levels of αGlcNAc in these lesions could serve as a biomarker to predict malignant potential and cancer progression.

The curious case of G\u03b1s gain-of-function in neoplasia

BackgroundMutations activating the α subunit of heterotrimeric Gs protein are associated with a number of highly specific pathological molecular phenotypes. One of the best characterized is the McCune Albright syndrome. The disease presents with an increased incidence of neoplasias in specific tissues.Main bodyA similar repertoire of neoplasms can develop whether mutations occur spontaneously in somatic tissues during fetal development or after birth.Glands are the most “permissive” tissues, recently found to include the entire gastrointestinal tract. High frequency of activating Gαs mutations is associated with precise diagnoses (e.g., IPMN, Pyloric gland adenoma, pituitary toxic adenoma). Typically, most neoplastic lesions, from thyroid to pancreas, remain well differentiated but may be a precursor to aggressive cancer.ConclusionsHere we propose the possibility that gain-of-function mutations of Gαs interfere with signals in the microenvironment of permissive tissues and lead to a transversal neoplastic phenotype.

Gastric pyloric gland adenoma: a multicentre clinicopathological study of 67 cases.

There is limited information regarding the clinicopathological and immunohistochemical characteristics of gastric pyloric gland adenomas (PGAs). Sixty-seven cases of gastric PGA from 57 patients were analysed. PGAs occurred with similar frequency in men and women (47.4 and 52.6%, respectively), with a mean age of 66 years. Most presented in the gastric body/fundus (67.2%). Fifteen cases (22.4%) developed against a background of autoimmune gastritis (AIG), whereas normal mucosa was seen in 35.8%. Only 16.4% (11 cases) developed in patients with a genetic predisposition, most commonly familial adenomatous polyposis. Low-grade lesions had a mean size of 1.5 cm, while PGAs with high-grade dysplasia (HGD) or adenocarcinoma had a mean size of 3.5 cm (P < 0.001) and more commonly showed tubulovillous architecture (50.0 versus 25.6% in low-grade dysplasia; P = 0.040). Most PGAs (61.2%) co-expressed mucin (MUC)5AC and MUC6 (mixed type), which was associated significantly with HGD or adenocarcinoma (P = 0.013). AIG was also associated with HGD (P = 0.027), but genetic predisposition did not correlate with the grade of dysplasia (P = 0.793). The recurrence rate of PGA was similar for high- (11.8%) and low-grade lesions (7.4%) (P = 0.624). The risk of HGD increases with the size of PGA, tubulovillous architecture and the presence of AIG as well as mixed immunophenotype. As the overall local recurrence rate is less than 10%, PGAs may be treated conservatively, but they should be excised completely if possible, particularly if they are large or show high-grade features.

Factors Associated With the Development of Gastric Cancer in FAP: 2017 Fellows-in-Training Award (Stomach Category): 2017 Presidential Poster Award

Introduction: Gastric cancer has not been described as a cancer risk in Western patients with FAP. Data demonstrates a recent and rapid increase in the incidence of gastric cancer (GC) in FAP patients. We performed a case control study to determine clinical and endoscopic factors associated with GC in FAP. Methods: FAP patients were identified through the IRB approved David G. Jagelman Inherited Colorectal Cancer Registries CologeneTM database. All FAP patients with GC and randomly selected FAP patients without GC with > 2 EGDs were analyzed. Demographic, clinical, endoscopic and pathologic features were compared. A p < 0.05 was considered statistically significant. Results: Ten (10) patients developed GC. Age at diagnosis of FAP, age at the last EGD or age at diagnosis of GC, race, gender, BMI, tobacco exposure, personal history of cancer (CRC, thyroid, duodenal), family history of CRC, and history of duodenal surgery were not different between cases and controls (Table 1). Patients with GC were more likely than controls to have desmoids (60% vs 16%, p < 0.001), PPI (90% vs 54%, p 0.029) and H2RA exposure (60% vs13%, p < 0.001). Patients with GC had a longer length of EGD surveillance (10.8 vs 6 years, p< 0.002) but similar intervals between EGDs (1.3 vs 2.3 years, p=0.21) as controls (Tables 1 & 2). Endoscopic features significantly associated with GC include a carpeting of proximal polyposis (100% vs 26%, p < 0.001), greater numbers and largest sizes of solitary proximal polyps and presence of a polypoid mound of proximal polyposis (all p < 0.001) (Table 2). The pathology of proximal polyps varied significantly between GC and controls including the presence of intestinal metaplasia (IM) (30% vs 2.9%, p=0.013), fundic gland polyps with low grade (100% vs 54%, p=0.006) and high grade dysplasia (FGPHGD) (40% vs 7%, p=0.002), pyloric gland adenomas with HGD (PGAHGD) (20% vs 0%, p=0.014) and tubular adenomas (TA) (30% vs 5.7%, p=0.011) (Table 3).Table: Demographics and Medical History.Table: EGD Surveillance.Table: EGD Findings.Conclusion: Endoscopic features associated with GC in FAP include a carpeting, large size and polypoid mounds of proximal gastric polyposis. Worrisome histologic features include FGPHGD and PGAHGD. FAP patients with concerning endoscopic features should undergo intensive surveillance, aggressive debulking of polypoid mounds in addition to random sampling of polyps. Prophylactic gastrectomy should be offered to those with endoscopically worrisome stomachs and any lesion with HGD.

Duodenal Pyloric Gland Adenoma in a 59-year-old Asian Male: A Case Report

Duodenal Pyloric Gland Adenoma in a 59-year-old Asian Male: A Case Report

Duodenal Neoplasms of Gastric Phenotype: An Immunohistochemical and Genetic Study With a Practical Approach to the Classification.

Duodenal neoplasm of gastric phenotype (DNGP) is very rare, and details of its histopathologic, genetic, and biological features are still unclear. Frequent gene mutations in GNAS, KRAS, and APC have been reported in pyloric gland adenomas and fundic gland-type neoplasms (initially reported as low-grade adenocarcinomas) of the stomach. Here we retrospectively analyzed 16 cases of extra-ampullary DNGP (benign to malignant), and we examined the mucin immunoprofile and oncogene mutations (GNAS, KRAS, APC, BRAF, and CTNNB1). The 16 DNGPs were histologically classified into adenomas (5 pyloric gland adenomas and 2 foveolar-type adenomas), neoplasms of uncertain malignant potential (NUMPs, n=6), and invasive adenocarcinomas (n=3). NUMPs consisted of slightly atypical epithelial cells with pale, eosinophilic, or basophilic cytoplasm growing in an anastomosing or branching glandular pattern, often with expansive submucosal extension. In contrast to invasive adenocarcinomas, NUMPs lacked significant nuclear irregularity, desmoplastic stromal reaction, lymphovascular invasion, and metastasis; their features were reminiscent of fundic gland-type neoplasms of the stomach. Immunophenotypically, most of NUMPs were predominantly positive for MUC6 with variable expressions of pepsinogen-I, HKATPase, human gastric mucin, and MUC5AC. Molecular analyses revealed the gene mutations of GNAS in 6 (38%) of 16 DNGPs (4 [57%] adenomas, 1 [16%] NUMP, and 1 [33%] invasive adenocarcinoma) and APC in 4 of 15 (27%) DNGPs: no adenomas, 2 (33%) NUMPs, and 2 (67%) invasive adenocarcinomas. BRAF mutation was present in only 1 (16%) NUMP, and KRAS and CTNNB1 mutations were absent. In conclusion, gastric-phenotype adenomas and NUMPs of the duodenum are similar to their counterparts of the stomach, in terms of histologic, genetic, and clinicopathologic features. We propose the term "NUMP" as an intermediate category between adenoma and definitely invasive adenocarcinoma. Our findings may provide novel insights into the classification of undescribed but distinctive duodenal tumors showing similarity to gastric-phenotype neoplasms of the stomach.

Precursors of gastric cancer : Dysplasia and adenoma

Gastric cancer develops from preneoplastic and early neoplastic precursor lesions. In particular, the intestinal type according to the Lauren classification is driven by chronic inflammation and progresses via achronic gastritis - atrophy/metaplasia - dysplasia - carcinoma sequence. Staging of the extent of atrophy (OLGA) or intestinal metaplasia (OLGIM) enables risk stratification and determines follow-up investigations according to the management of precancerous conditions and lesions in the stomach (MAPS) international guidelines. True adenomatous lesions are relatively rare in the stomach. Three major types need to be considered: the intestinal type (tubular, tubulovillous and villous), the foveolar type (with superficial gastric differentiation) and the pyloric gland adenoma (with deep gastric differentiation). The intestinal type is the most common and needs to be differentiated from nonneoplastic polypoid regenerative hyperplasia, but also from well-differentiated tubular adenocarcinoma.

A case of gastric adenocarcinoma with a component of pyloric gland adenoma arising in stomach probably uninfected with Helicobacter pylori

A case of gastric adenocarcinoma with a component of pyloric gland adenoma arising in stomach probably uninfected with <I>Helicobacter pylori</I>

Morphology and genetics of pyloric gland adenomas in familial adenomatous polyposis.

Gastric pyloric gland adenomas (PGAs) are rare epithelial polyps that are found more commonly in autoimmune atrophic gastritis and familial adenomatous polyposis (FAP). Little is known about the morphology and genetics of PGAs in FAP. PGAs in FAP are studied morphologically and genetically. Findings in FAP-associated PGAs are compared to sporadic PGAs and related lesions such as oxyntic gland adenoma (OGA) to increase our understanding of these rare polyps. Seven PGAs and 18 fundic gland polyps (FGPs) from FAP patients were collected. KRAS and GNAS mutations were determined in six PGAs and 18 FGPs. Immunohistochemistry was applied on five PGAs to provide further confirmation of the histological subtypes and genetic alterations. Morphology of all PGAs was studied and compared to literature on sporadic PGAs and related lesions. All successfully sequenced PGAs (six of six) carried GNAS mutations and half of the successfully sequenced PGAs carried a KRAS mutation (three of six). Nuclear β-catenin was seen only in one PGA with focal high-grade dysplasia. Morphologically, PGAs in FAP showed overlapping features with OGA. Familial adenomatous polyposis-associated PGAs have a similar genetic background as sporadic PGAs, i.e. KRAS and GNAS mutation. Based on morphological findings in FAP associated PGAs, it is hypothesized that PGAs and OGAs are closely related lesions.

Decreased expression of gastric gland mucin-specific glycan α1,4-linked N-acetylglucosamine on its scaffold mucin 6 is associated with malignant potential of pyloric gland adenoma of the stomach.

Pyloric gland adenoma (PGA) is a unique gastric neoplasm expressing mucin 6 (MUC6), and is often associated with high-grade dysplasia and/or adenocarcinoma. MUC6 secreted from the gastric gland mucous cells, such as pyloric gland cells, carries unique O-glycans with terminal α1,4-linked N-acetylglucosamine (αGlcNAc) residues on its molecule. As we recently demonstrated that αGlcNAc serves as a tumour suppressor for gastric adenocarcinoma, this study aimed to investigate the significance of αGlcNAc expression in PGA. Eighteen patients with PGA were examined with immunohistochemistry for αGlcNAc and MUC6. αGlcNAc and MUC6 were coexpressed in 12 of 18 PGAs. However, reduced αGlcNAc expression relative to MUC6 expression was observed in six cases. When the MIB-1 labelling index (LI) of tumour cells was examined with respect to reduced αGlcNAc expression, the MIB-1 LI was significantly higher in PGAs showing decreased αGlcNAc expression relative to MUC6 expression than in PGAs with unchanged αGlcNAc expression (P = 0.023). The present study indicates that coexpression of αGlcNAc and MUC6 in PGA suggests the presence of fully glycosylated MUC6 on tumour cells, consistent with pyloric gland differentiation. However, the decreased glycosylation of αGlcNAc on MUC6 is associated with high mitotic activity of tumour cells, indicative of malignant potential of PGA.

Gastric pyloric gland adenoma.

Pyloric gland adenomas are rare neoplasms of the gastrointestinal tract. Gastric pyloric gland adenomas have been shown to arise in chronically damaged mucosa. The neoplastic glands have gastric pyloric gland differentiation and have a tightly packed organization with occasional cystic dilatation. The individual cells are cuboidal to columnar, with eosinophilic to amphophilic cytoplasm and either no apical mucin cap or a poorly formed apical mucin cap. The nuclei are round to oval, with occasional prominent nucleoli. Immunohistochemically, the neoplastic cells label with markers of gastric pyloric gland differentiation, including MUC6 and MUC5AC. There is limited information regarding the natural history of pyloric gland adenomas, but clinical series have described adenocarcinomas in association with gastric pyloric gland adenomas. The ideal clinical management is adequate sampling of the lesion to investigate for high-grade dysplasia and/or invasive cancer and recommendation to clinical colleagues to investigate the background mucosa for the etiology of chronic gastritis as well as potential additional neoplastic lesions. This review will focus on gastric pyloric gland adenomas.