BACKGROUND: Recently OLGA (Operative Link on Gastritis Assessment) classification has been proposed to identify high-risk forms of gastritis that can evolve in gastric cancer (stages III and IV). Helicobacter pylori infection and age older than 40 have been considered as independent risk factor for high-risk OLGA stages

Alvaro, Domenico

Cannaviello, Claudio

Efrati, Cesare

Finizio, Roberto

Giulitti, Diego

Mangogna, LIVIA MARIA

o Sed, Nicole Piazza

Ridola, Lorenzo

Taccogna, Silvia

Valabrega, Stefano

English

Cesare Efrati

Claudio Cannaviello

Livia Maria Mangogna

stefano valabrega

Lorenzo Ridola

Domenico Alvaro

Diego Giulitti

Nicole Piazza o Sed

Silvia Taccogna

Roberto Finizio

Crossref

Gastroenterology

The Staging of Gastritis with the Olga System in the Italian Setting: Histological Features and Gastric Cancer Risk

Stefano Valabrega

Archivio della ricerca- Università di Roma La Sapienza

Su1115THE STAGING OF GASTRITIS WITH THE OLGA SYSTEM IN THE ITALIANSETTING: HISTOLOGICAL FEATURES AND GASTRIC CANCER RISKCesare Efrati, Claudio Cannaviello, Livia Maria Mangogna, stefano valabrega, LorenzoRidola, Domenico Alvaro, Diego Giulitti, Nicole Piazza o Sed, Silvia Taccogna, RobertoFinizioBACKGROUND: Recently OLGA (Operative Link on Gastritis Assessment) classification hasbeen proposed to identify high-risk forms of gastritis that can evolve in gastric cancer (stagesIII and IV). Helicobacter pylori infection and age older than 40 have been considered asindependent risk factor for high-risk OLGA stages. OBJECTIVE: The aim of this study wasto confirm the role of OLGA staging in identifying patients at risk. METHODS: This is aretrospective study. Data were collected from records of endoscopy unit database. SPSSstatistical software was used for all computations. PATIENTS: We analyzed 520 gastricbiopsies from patients who underwent esophagogastroduodenoscopy for gastric cancerscreening. Patients were subsequently classified as stage I-IV according to OLGA system andthey were also clustered according to age, complete and incomplete metaplasia and atrophy.RESULTS: 156 M/354F, age 62.4±12.6 were included in the study. The distribution ofhistological features of gastric biopsies are reported in table 1. Complete metaplasia (269/284, p 0.01), gastric atrophy (343/367, p 0.005) and a grade of OLGA staging ≥ II (335/356, p 0.009) were prevalent in subjects older than 40 years old, as well as Helicobacterpylori infection tended to be higher (136/149 p ns). CONCLUSION: High-risk forms ofgastritis according to OLGA staging system are significantly associated not only to H. pyloriinfection, but also to older age, gastric atrophy and complete metaplasia. That results canconfirm the importance of OLGA system in order to identify patients at risk, requiringmore surveillance.OLGA 0: well visible glands, occupying the entire mucosal layerX : 14740$CH0103-15-17 11:16:44 Page 473PDFd : 14740B : oS-473 AGA AbstractsOLGA IV: glands are totally disappeared; we can also observe diffuse intestinal completemetaplasia and hypertrophic muscolaris mucosae.Su1116GASTRIC INTESTINAL METAPLASIA TYPE III AND PROSPECTIVE RISKOF GASTRIC CANCER IN COLOMBIAM. Blanca Piazuelo, M. Constanza Camargo, Robertino M. Mera, Alberto G. Delgado,Juan C. Bravo, Richard M. Peek, Pelayo Correa, Douglas Morgan, Luis E. Bravo, Keith T.WilsonBackground: In the Correa model of gastric carcinogenesis, Helicobacter pylori causes chronicgastritis, which over time may progress through the premalignant stages of atrophic gastritis,intestinal metaplasia (IM), and dysplasia, to finally gastric cancer (GC). Extension and typesof IM have been associated with differential GC risk. Our study evaluated the associationbetween type III IM (a subtype of incomplete IM with sulfomucin-positive columnar cells)and prospective risk of GC in a cohort of individuals from a high-risk area in Colombia.Methods: 795 subjects with gastric precancerous lesions were randomized to anti-H. pyloritreatment or placebo at enrollment. Gastric biopsies at baseline were scored according toour validated histopathology scoring system. Ten individuals developed GC during 16 yearsof follow-up (median time to GC, 8 years, interquartile range, 3-12). Three controls wereselected for each GC case, matched for age, sex, histopathology score at baseline, anti-H.pylori treatment at baseline, and length of follow-up. Sections from all biopsies with IMwere stained with high-iron diamine/Alcian blue (HID-AB). IM was initially classified intocomplete and incomplete types, assessing percentages of epithelium replaced with either IMtype. The percentage of epithelium containing sulfomucin-positive columnar cells wasassessed in HID-AB sections. All evaluations were performed semiquantitatively by a patholo-gist blinded to clinical information. The maximum value obtained in a single biopsy acrossthe set of biopsies for each subject was considered for the analyses comparing GC casesand controls. To assess differences in anatomic location of IM, biopsies were grouped intoantrum (including incisura) and corpus. Conditional logistic regression models were usedto estimate odds ratios (OR). Results: All individuals who developed GC had IM at baseline.As a result of the case-control matching, there were no statistically significant differencesin extension of complete-type (p=0.86) or incomplete-type (p=0.43) IM. Notably, greaterexpression of sulfomucins at baseline, was associated with increased GC risk (adjusted OR=1.29, 95% CI, 1.02-1.63 for each increment in 5% on the expression of sulfomucins). Inanatomic location-specific analyses, mean extensions of sulfomucins, total and subtype IMwere greater in the antrum as compared to the corpus: 6% vs. 1% for sulfomucins (p=0.003), 53% vs. 22% (p<0.001) for total 7% vs. 19% for complete-type (p=0.01), and 17%vs. 3% for incomplete-type (p<0.001), regardless of case-control status. Conclusions: AllIM lesions were more extensive in the antrum. Assessment of sulfomucin expression ingastric IM is useful for the identification of patients at higher risk of GC. This strategy couldprove useful to determine which individuals with IM may benefit from closer endoscopic sur-veillance.Su1117AUTOPHAGIC PROTEINS AS MARKERS OF DYSPLASTIC CHANGES INGASTRIC MUCOSAJu-Yoon Yoon, Catherine StreutkerGastric adenocarcinomas remain a difficult disease to treat, and early recognition remainsa key. Early detection of low-grade dysplasia (LGD) and risk stratification of LGD casesbecomes important for improved management, considering the relatively rapid progressionof high-grade dysplasia (HGD) to carcinoma. Metabolic dysregulation, including autophagy,is a phenomenon with well-recognized contribution to carcinogenesis, and we aimed toexamine autophagy by examining the level and distribution of p62, LC3B and LAMP2A.We examined a total of 36 cases of gastric mucosa (biopsy and resection) by immunohistoche-mistry (IHC). The obtained staining intensity and staining patterns were compared betweengastric specimens with histologically confirmed cases of normal, dysplasia and adenocarci-noma. p62 and LC3 proteins could be readily detected in the cytoplasm in the gastricmucosa by IHC. Cytoplasmic p62 staining intensity was higher in the specimens withdysplasia (33.3-40% with 3+ staining vs. 0% in intestinal metaplasia and normal mucosa).This trend was not observed with cytoplasmic LC3 staining intensity. LAMP2A stainingexhibited mostly punctate pattern, and the staining intensity was not discriminating betweenthe different histological categories. Nucleocytoplasmic shuttling of p62 and LC3 has beenpreviously described, and we observed nuclear staining in the gastric mucosa. Lower nuclearp62 was seen in adenocarcinoma in comparison to cases with dysplasia (66.7% with 0+staining in adenocarcinoma vs. 10% in dysplasia). A similar but less dramatic trend wasobserved with nuclear LC3 (25% with 0+ staining in adenocarcinoma vs. 0-9.1% in othercategories). in vitro works have placed ErbB family members, including EGFR and ErbB2/HER2, as upstream modulators of autophagy. In our cohort, 2/6 cases of adenocarcinomawere positive for ERBB2 amplification, and these cases concordantly exhibited highest cyto-plasmic p62 staining compared to other adenocarcinoma cases. When we examined themRNA levels in gastric adenocarcinoma cases from The Cancer Genome Atlas (TCGA), wefound an interesting series of positive correlations between ERBB2 mRNA levels and a numberof autophagy-related genes, including BECN1 (Spearman rho = 0.2449, p < 0.0001) andp62/SQSTM1 (rho = 0.1329, p = 0.0067), while correlating negatively with MAP1LC3A (rho =-0.1079, p = 0.0279). This pattern of correlations was not observed with EGFR mRNA levels.Taken together, an interesting role for autophagy in gastric adenocarcinoma pathogenesisis suggested by the combined IHC and mRNA data. As in cases of HER2-positive breastcancers, p62 levels appear to be higher in HER2-positive gastric adenocarcinoma. It is unclearwhether the cytoplasmic accumulation of p62 can be equated with decreased autophagy,and further work is underway to tease out the clinical significance of our findings.AGAAbstracts

The staging of gastritis with the olga system in the italian setting. histological features and gastric cancer risk

https://iris.uniroma1.it/bitstream/11573/1063954/1/Efrati_Staging_2017.pdf

The staging of gastritis with the olga system in the italian setting. histological features and gastric cancer risk

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Archivio della ricerca- Università di Roma La Sapienza