Gastritis OLGA‐staging and gastric cancer risk: a twelve‐year clinico‐pathological follow‐up study

Rugge, Massimo; Boni, Michele De; Pennelli, Gianmaria; Bona, Manuela De; Giacomelli, Luciano; Fassan, Matteo; Basso, Daniela; Plebani, Mario; Dy, Graham

doi:10.1111/j.1365-2036.2010.04277.x

Cited by 233 publications

(200 citation statements)

References 40 publications

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“…The mean pepsinogen I ⁄ II ratio was correlated with respective result of the OLGA stage. The assessment of the OLGA stage at inclusion allows us to predict the OLGA stage at the end point as well as the incidence of neoplasia [36].…”

Section: H Pylori As High Risk Indicatormentioning

confidence: 99%

Gastric Cancer: Clinical Aspects, Epidemiology and Molecular Background

et al. 2011

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In 2010, the WHO introduced the seventh edition of the tumor node metastasis (TNM) classification that provides a more detailed classification for both local tumor invasion (T) and lymph node involvement (N) compared with the previous version. The T and N categories of tumors located in the stomach have been further modified with the intention to ensure a better correlation to the prognostic outcome. For the classification of a pN0, the number of lymph nodes has been adjusted to 16.The description of tumors with origin in the esophagus has been simplified and includes tumors of the esophagogastric junction as well as gastric tumors extending to the proximal 5 cm of the stomach. Major changes are further the subclassification of the categories T1 and T4 and the new N categorization now considering the number of lymph nodes involved within tree categories. Furthermore, positive lymph nodes in the region of the celiac trunc are considered as regional in case of esophageal cancers.The validity of the new classification system in its prognostic efficacy was compared to the previous edition. A study conducted in China proved a better prognostic stratification for the new actualized version [1]. Another study from Korea showed similar results for the new TNM system, proving a more detailed prognostic assessment, especially between T2 and T3 and N1 and N2 tumors [2]. The advantage of the new (7th) edition was mainly confirmed for the prognostic value of accurate lymph node assessment [3].Concerning the classification of early gastric cancer (GC) in the new system, a study from Italy confirmed the usefulness of the new classification for metastatic lymph nodes as a prognostic tool in case of early GC. AbstractThe validity and usefulness of the 7th edition of the UICC tumor node metastasis classification in the context of clinical management of gastric cancer are discussed. The most relevant new agent in gastric cancer therapy is trastuzumab for HER2-positive gastric carcinomas. This marks the success of continuous effort of translational research. Trastuzumab, initially applied in palliative settings, is currently being evaluated also in neoadjuvant treatment regimens. Several new meta-analyses support the carcinogenic effect of high salt intake and smoking in the context of Helicobacter pylori infection. Further data have become available on the efficacy of protective agents, acetyl salicylic acid ⁄ nonsteroidal anti-inflammatory drugs, and antioxidants. In search for a successful prevention strategy, the focus is on the identification of individuals at high risk who demand screening (testing) and surveillance. Serological assessment of gastric mucosal abnormalities with increased risk for gastric cancer development is extensively studied, and new data are presented from Asia as well as from Europe. New high-throughput techniques combined with bioinformatic vector analysis open the gate to the identification of new potential diagnostic and therapeutic targets. Furthermore, these approaches allow us to elucidate the int...

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Section: H Pylori As High Risk Indicatormentioning

confidence: 99%

Gastric Cancer: Clinical Aspects, Epidemiology and Molecular Background

et al. 2011

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“…The series included: 1) normal gastric oxyntic mucosa obtained from dyspeptic patients, as control (n = 10); 2) mucosa from H. pylori 2 nonatrophic chronic gastritis (n = 10); 3) mucosa from H. pylori + nonatrophic chronic gastritis, before H. pylori eradication therapy (ET; n = 10); and 4) mucosa from the same patients as in 3), who underwent clinical and histological remission, after H. pylori ET. H. pylori was assessed by histology (modified Giemsa staining) and confirmed by clinical history, rapid urease testing, and/or ELISA (H. pylori-specific IgG Abs; GastroPanel, Biohit HealthCare, Milan, Italy) (13). Two trained gastrointestinal pathologists, blinded to any of the patients' endoscopic or clinical information, jointly assessed the original slides (H&E, Alcian blue-periodic acid schiff, and Giemsa for H. pylori).…”

Section: Patientsmentioning

confidence: 99%

Cytokine BAFF Released byHelicobacter pylori–Infected Macrophages Triggers the Th17 Response in Human Chronic Gastritis

Munari

Fassan

Capitani

et al. 2014

The Journal of Immunology

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BAFF is a crucial cytokine that affects the activity of both innate and adaptive immune cells. It promotes the expansion of Th17 cells in autoimmune disorders. With this study, we investigated the BAFF/Th17 responses in Helicobacter pylori–induced gastritis in humans. Our results show that the mucosa from Helicobacter+ patients with chronic gastritis is enriched in IL-17 and BAFF, whereas the two cytokines are weakly expressed in Helicobacter− patients with chronic gastritis; moreover, the expression of both BAFF and IL-17 decreases after bacteria eradication. We demonstrate that BAFF accumulates in macrophages in vivo and that it is produced by monocyte-derived macrophages in vitro, after Helicobacter stimulation. Application of BAFF on monocytes triggers the accumulation of reactive oxygen species that are crucial for the release of pro-Th17 cytokines, such as IL-23, IL-1β, and TGF-β. Moreover, BAFF directly promotes the differentiation of Th17 cells. In conclusion, our results support the notion that an axis BAFF/Th17 exists in chronic gastritis of Helicobacter+ patients and that its presence strictly depends on the bacterium. Moreover, we demonstrated that BAFF is able to drive Th17 responses both indirectly, by creating a pro-Th17 cytokine milieu through the involvement of innate immune cells, and directly, via the differentiation of T cells toward the specific profile. The results obtained in this study are of great interest for Helicobacter-related diseases and the development of novel therapeutic strategies based on the inhibition of the BAFF/IL-17 response.

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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%

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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Gastritis OLGA‐staging and gastric cancer risk: a twelve‐year clinico‐pathological follow‐up study

Cited by 233 publications

References 40 publications

Gastric Cancer: Clinical Aspects, Epidemiology and Molecular Background

Gastric Cancer: Clinical Aspects, Epidemiology and Molecular Background

Cytokine BAFF Released byHelicobacter pylori–Infected Macrophages Triggers the Th17 Response in Human Chronic Gastritis

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

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