Gastritis: The histology report

Pennelli, Gianmaria; Pilozzi, Emanuela; Fassan, Matteo; Ingravallo, Giuseppe; Russo, Valentina; Mario, F. Di

doi:10.1016/s1590-8658(11)60593-8

Cited by 131 publications

(131 citation statements)

References 42 publications

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“…The gross features of the tumor were obtained from both the gross description of the specimen as recorded at the time of surgery and from the original histopathology report. All EGCs were located in stomachs that had stage III-IV atrophic gastritis, according to Operative Link on Gastritis Assessment (OLGA) classification [3,10], and presented a HG-IEN lesion distinct from the EGC lesion. The extension of gastric mucosa atrophy and intestinal metaplasia was assessed histologically from the original hematoxylin and eosin (H&E) slides.…”

Section: Casesmentioning

confidence: 99%

“…All biopsies were taken from the distal gastric mucosa, i.e., antrum and/or incisura angularis, and included (1) 15 biopsies of normal antral mucosa, obtained from dyspeptic patients; (2) 15 biopsies of antral mucosa with extensive intestinal metaplasia, obtained from cases of atrophic gastritis in OLGA stages III-IV [3,10] Original H&E slides were jointly reevaluated and reclassified according to WHO 2010 criteria [11] by two GI pathologists (M.F., C.L. ), blinded to all clinical and pathological information; two additional expert pathologists (P.C., A.T.) evaluated cases of discordant classification.…”

Section: Casesmentioning

confidence: 99%

“…Intestinal-type adenocarcinoma is the final outcome of long-standing gastritis caused primarily by Helicobacter pylori infection [2]. Chronic gastritis leads to the replacement of the native epithelium with intestinal metaplasia, the 'carcinogenic field' in which initially dysplastic lesions and subsequently adenocarcinomas may develop [3].…”

Section: Introductionmentioning

confidence: 99%

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High-throughput mutation profiling identifies novel molecular dysregulation in high-grade intraepithelial neoplasia and early gastric cancers

et al. 2013

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Background There is still no widely accepted molecular marker available to distinguish between gastric high-grade intraepithelial neoplasia (HG-IEN) and invasive early gastric cancer (EGC). Methods HG-IEN and EGC lesions coexisting in the same patient were manually microdissected from a series of 15 gastrectomies for EGC; 40 ng DNA was used for multiplex PCR amplification using the Ion AmpliSeq Cancer Panel, which explores the mutational status of hotspot regions in 50 cancer-associated genes. Results Of the 15 EGCs, 12 presented at least one somatic mutation among the 50 investigated genes, and 6 of these showed multiple driver gene somatic mutations. TP53 mutations were observed in 9 cases; APC mutations were identified in 3 cases; and ATM and STK11 were mutated in 2 cases. Seven HG-IEN lesions shared an identical mutational profile with the EGC from the same patient; 13 mutations observed in APC, ATM, FGFR3, PIK3CA, RB1, STK11, and TP53 genes were shared by both HG-IEN and ECG lesions. CDKN2A, IDH2, MET, and RET mutations were observed only in EGC. TP53 deregulation was further investigated in an independent series of 75 biopsies corresponding to all the phenotypic lesions occurring in the EGC carcinogenetic cascade. p53 nuclear immunoreaction progressively increased along with the dedifferentiation of the lesions (P \ 0.001). Overall, 18 of 20 p53-positive lesions showed a TP53 mutated gene. Discussion Our results support the molecular similarity between HG-IEN and EGC and suggest a relevant role for TP53 in the progression to the invasive phenotype and the use of immunohistochemistry as a surrogate to detect TP53 gene mutations.

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Section: Casesmentioning

confidence: 99%

Section: Casesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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High-throughput mutation profiling identifies novel molecular dysregulation in high-grade intraepithelial neoplasia and early gastric cancers

et al. 2013

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“…Chronic atrophic gastritis, intestinal metaplasia, and dysplasia are included in premalignant gastric lesions, but only atrophy and intestinal metaplasia are included in the assessment of gastritic degrees according to the Updated Sydney System, which is the degree of gastritis accepted universally by the Anatomical Pathologist in the world. 23 The risk of having higher MDA levels was greater in patients with both moderate + severe atrophy and intestinal metaplasia compared to those with moderate + severe neutrophil activity. This indicated that elevation of MDA level was an important parameter for detecting severe tissue damage, and it has been reported from previous studies that MDA level were associated with mutagenesis and carcinogenesis.…”

mentioning

confidence: 90%

Association Between Degree of Gastritis and Malondialdehyde Level of Gastritis Patients at Adam Malik General Hospital Medan

Darmadi

Siregar

Dairi

2020

InaJGHE

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Background: The main pathogenesis of gastritis is inflammation which process can not be separated from the role of free radicals. Malondialdehyde (MDA) is a free radical biomarker and which increases in gastritis (p = 0.014; PR = 8.667;). There was a significant association between degree of neutrophil activity with high MDA level (p = 0.002; PR = 11.33;). There was a significant association between degree of atrophy with high level of MDA (p < 0.001; PR = 14;). There was a significant association between degree of intestinal metaplasia with high MDA level (p = 0.001; PR = 12.5;.Conclusion: There were significant associations between degree of lymphocyte infiltration, neutrophil activity, atrophy, and intestinal metaplasia with high level of MDA.

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“…A continuación analizamos el perfil de sobreexpresión de p73 y otros genes (BRCA1, HSP90, STAT1, FHIT, EGFR, p53, p16INK4a) asociados a activación por hipometilación [71][72][73][74][75][76][77][78][79] en microarreglos de tejidos (TMA, tissue microarray) de cáncer gástrico (mucosa gástrica tumoral y mucosa adyacente al tumor, n = 91) y gastritis (n = 148). En forma paralela a este análisis evaluamos las característi-cas histológicas de los casos según el sistema de Sydney para gastritis crónica y OLGA (Operative Link on Gastritis Assessment) para la evaluación de atrofia 80,81 . El análisis histológico nos permitió identificar atrofia y metaplasia intestinal severa rev Med chile 2013; 141: 1570-1577 epigenética y biomarcadores en cáncer gástrico -a. corvalán en la mayoría de las mucosas adyacentes a tumor en comparación con los casos de gastritis.…”

Section: Hipometilación Del Adn Y Cáncer Gástricounclassified

Bases epigenéticas del cáncer gástrico: oportunidades para la búsqueda de nuevos biomarcadores

2013

Rev. méd. Chile

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Epigenetics in the pathogenesis and early detection of gastric cancerpuc.cl E l cáncer gástrico es la primera causa de muerte por enfermedades neoplásicas en Chile y la segunda en el mundo 1,2 . A pesar de los avances en el tratamiento y una disminución de sus lesiones precursoras 3,4 , recientes publicaciones sugieren un probable aumento de su mortalidad, particularmente en población joven 5 . Estas observaciones, en conjunto con proyecciones de la mortalidad global para los próximos 20 años, sugieren que el cáncer gástrico ocupará la décima causa global de muerte para la década del 2030 6 . El cáncer gástrico se puede clasificar según aspectos clínicos, endoscópicos o histológicos 7-13 . La clasificación más utilizada es la propuesta por Lauren 13 , la cual, según parámetros histológicos, define dos tipos de cáncer gástrico: el intestinal y el difuso. El primero se caracteriza por la formación de estructuras glandulares que semejan la mucosa colónica y que está precedida por una secuencia de lesiones muy bien caracterizadas por Correa y col. 14,15 . Por otra parte, el cáncer gástrico de tipo difuso, no forma estructuras histológicas y en consecuencia no tiene lesiones precursoras reconocidas 16 . Una particularidad importante de la clasificación de Lauren es que ha sido muy útil para estudiar el rol del ambiente, en particular en la variante intestinal 15 . En este sentido, las lesiones precancerosas han demostrado progresar de forma dinámica, desde la gastritis crónica superficial, gastritis crónica atrófica, metaplasia intestinal y finalmente displasia. Estos eventos constituyen las bases del "modelo humano de cáncer gástrico" postulado por Correa 17 . Una de las características fundamentales de este modelo es que junto con identificar una secuencia progresiva de lesiones, señala también la existencia de progresión/regresión de estas lesiones.

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Gastritis: The histology report

Cited by 131 publications

References 42 publications

High-throughput mutation profiling identifies novel molecular dysregulation in high-grade intraepithelial neoplasia and early gastric cancers

High-throughput mutation profiling identifies novel molecular dysregulation in high-grade intraepithelial neoplasia and early gastric cancers

Association Between Degree of Gastritis and Malondialdehyde Level of Gastritis Patients at Adam Malik General Hospital Medan

Bases epigenéticas del cáncer gástrico: oportunidades para la búsqueda de nuevos biomarcadores

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