scholarly journals Sa1956 Old Age Is Another Independent Risk Factor for Metachronous Gastric Cancer Irrespective of H. pylori Eradication; Retrospective, Single Tertiary Center Study

2014 ◽  
Vol 146 (5) ◽  
pp. S-339
Author(s):  
SeongWoo Jeon ◽  
Yong-hwan Kwon
2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Zhi-Yi Zhou ◽  
Jie Sun ◽  
Qing Guo ◽  
Hai-Bin Zhao ◽  
Zhi-Hua Zhou

Abstract Background Certain gastric cancers exhibit some primitive phenotypes, which may indicate a high malignancy. In histologically differentiated early gastric cancer (EGC), the presence and the clinicopathological significance of the primitive phenotype remain unclear. Methods Using immunohistochemical staining we detected the expression of three primitive phenotypic markers SALL4, Glypican-3(GPC3), and AFP in whole tissue sections of differentiated EGC (gastrectomy specimens, n = 302). For those cases with primitive phenotypes, we analyzed their clinicopathological features and evaluated whether the criteria for endoscopic resection were met. Results We found that 9.3% (28/302) of all differentiated EGC cases have primitive phenotypes, and most of these cases (25/28) exhibit a histomorphology similar to conventional differentiated EGC. Patients with primitive phenotypes had a deeper invasion, a higher rate of ulcer and lymphatic invasion than cases without primitive phenotype. Moreover, patients with primitive phenotypes displayed a significantly higher frequency of LNM than those without (57.1% vs 8.8%, P < 0.001). Multivariate analysis revealed that presence of primitive phenotypes was an independent risk factor for LNM (P = 0.001, HR 6.977, 95% CI: 2.199–22.138). Interestingly, we found 2 cases with primitive phenotypes developed LNM, and they both met the expanded indications of endoscopic resection for differentiated EGC. Conclusions A small number of differentiated EGC have primitive phenotypes, which were closely related to LNM and were an independent risk factor for LNM. Given its highly aggressive behavior, differentiated EGC with primitive phenotypes should be evaluated with stricter criteria before endoscopic resection, or considered to give an additional surgical operation after endoscopic resection.


2011 ◽  
Vol 2 (6) ◽  
pp. 1197-1202 ◽  
Author(s):  
IK-CHAN SONG ◽  
ZHE-LONG LIANG ◽  
JUNG-CHAN LEE ◽  
SONG-MEI HUANG ◽  
HA-YON KIM ◽  
...  

2019 ◽  
Vol 37 (5) ◽  
pp. 381-393 ◽  
Author(s):  
Jan Bornschein ◽  
Elizabeth L. Bird-Lieberman ◽  
Peter Malfertheiner

While the primary risk factor for oesophageal adenocarcinoma (OAC) and its precursor lesion Barrett’s oesophagus (BO) is gastro-oesophageal reflux, the infection with Helicobacter pylori (H. pylori) is the dominant risk factor for gastric cancer. Reduction of reflux by dietary measures and proton pump inhibitors has some merits in OAC prevention, and the chemopreventive effect of Aspirin and statins is being widely investigated; however, improved outcome in OAC occurs primarily as the result of secondary prevention. Early detection of neoplastic lesions in Barrett’s metaplasia can be achieved by surveillance endoscopies. Novel endoscopic imaging modalities carry similar importance as the endoscopic treatment techniques as without detection of early lesions, therapy cannot be applied. Minimally invasive approaches are currently being investigated to identify patients with BO who are at particular risk of neoplastic progression. While dietary factors also play an important role in the prevention of gastric cancer and chemoprevention seems to be promising, the most beneficial effect has been shown for the eradication of H. pylori infection, which results in at least a one third reduction of gastric cancer risk. This effect can be further improved if the eradication takes place prior to the development of pre-neoplastic gastric conditions such as mucosal atrophy or intestinal metaplasia (IM). The definition of the “point of no return”, after which eradication is less effective, is of high importance, although H. pylori eradication can still be beneficial even at more advance stages of mucosal changes. For this reason, patients with advanced atrophy and IM should undergo endoscopic surveillance in the same way as patients with BO. There is also need for development of non-invasive tests to identify patients at high risk of progression to gastric cancer to improve outcome of these surveillance approaches.


2015 ◽  
Vol 33 (3_suppl) ◽  
pp. 19-19 ◽  
Author(s):  
Hayato Omori ◽  
Yuichiro Miki ◽  
Wataru Takagi ◽  
Fumiko Hirata ◽  
Taichi Tatsubayashi ◽  
...  

19 Background: Peritoneal recurrence is often observed in gastric cancer patients without serosal invasion. It is difficult for pathologists to evaluate whether tumor cells penetrate serosa or not, because the subserosa layer is very thin. We evaluated the incidence and risk factors of peritoneal recurrence in serosa -negative gastric cancer patients to clarify the mechanism of peritoneal recurrence in these patients. Methods: A total of 1,745 gastric cancer patients underwent R0 resection from 2002 to 2009 were enrolled. The incidence of peritoneal recurrence according to tumor depth was analyzed. In serosa-nagative patients, the univariate and multivariate analysis were performed to identify the risk factors for peritoneal recurrence. Results: Peritoneal recurrence was observed in 64 (3.7 %) out of 1,745 patients. The incidence of peritoneal recurrence according to depth of tumor invasion was in 0 / 466 in T1a, 5 / 567 (0.88 %) in T1b, 4 / 187 (2.1 %) in T2, 31 / 360 (7.9 %) in T3, 20 / 108 (15.9 %) in T4a, and 4 / 12 (25 %) in T4b, respectively (p<0.001). As for the risk factor for peritoneal recurrence in T3 patients, histologically undifferentiated type, negative lymphatic invasion, scirrhous type, invasive infiltrating growth pattern were the significant factors identified by univariate analysis. Only the invasive infiltrating growth pattern (OR3.44 p0.038) was selected as significant independent risk factor for peritoneal recurrence by multivariate analysis. In T1b / T2 patients, massive lymph node metastasis (N3a, 3b), scirrhous type were the significant factor for peritoneal recurrence by univariate analysis. Only massive lymph node metastasis (OR25.1 p<0.001) was selected as the significant independent risk factor by multivariate analysis. Conclusions: The incidence of peritoneal recurrence increases in proportion to the tumor depth. Invasive infiltrating growth pattern was selected as an independent risk factor for peritoneal recurrence in T3 patients, while it was massive lymph node metastasis in T1b / T2 patients. The results suggest the possibility that microscopic serosal invasion in T3 tumor and lymphatic progression in T1b / T2 tumor may contribute to peritoneal recurrence in gastric cancer.


2016 ◽  
Vol 31 (5) ◽  
pp. 959-964 ◽  
Author(s):  
Taisuke Imamura ◽  
Shuhei Komatsu ◽  
Daisuke Ichikawa ◽  
Toshiyuki Kosuga ◽  
Kazuma Okamoto ◽  
...  

2017 ◽  
pp. 47-52
Author(s):  
Thi Minh Thi Ha ◽  
Van Huy Tran ◽  
Viet Nhan Nguyen

Background: The interaction of environment factor and host factor plays the important role in the pathogenesis of gastric cancer (GC). This study aimed to evaluate the association of the combination of TP53 gene codon 72 polymorphism and the H. pylori infection with GC risk. Patients and methods: 112 patients with GC and 136 patients without GC were extracted DNA from specimens of gastric mucosa, then were determined TP53 gene codon 72 polymorphism by PCR-RFLP and diagnosed H. pylori infection by PCR with ureC gene-specific primers. Results: There was no significant association between TP53 gene codon 72 polymorphism and GC risk, as well as between H. pylori infection and GC risk. The combination of two factors (TP53 gene codon 72 polymorphism and H. pylori infection) was found to be associated with GC risk: The combination of Pro/Pro genotype and H. pylori (+) was the GC risk factor, OR = 2.62 (95%CI: 1.20–5.71) as compared to other combinations. In the group of H. pylori-positive patients, Pro/Pro genotype was the GC risk factor, OR = 2.42 (95%CI: 1.05 – 5.59) as compared to (Arg/Arg + Arg/Pro) group, and OR = 3.48 (95%CI: 1.23 – 9.78) as compared to Arg/Arg genotype. Conclusion: The factors of TP53 gene codon 72 polymorphism and H. pylori infection were not associated with GC risk as assessed separately, but they had the interaction associated with GC risk. Key words: TP53 gene codon 72 polymorphism, Helicobacter pylori, gastric cancer


2018 ◽  
Vol 154 (6) ◽  
pp. S-504-S-505
Author(s):  
Tomoari Kamada ◽  
Ken Haruma ◽  
Noriaki Manabe ◽  
Jiro Hata ◽  
Akiko Shiotani ◽  
...  

2015 ◽  
Vol 110 ◽  
pp. S1031
Author(s):  
Akinori Shimayoshi ◽  
Shunsuke Yamamoto ◽  
Shinjiro Yamaguchi ◽  
Kazuhiro Kozumi ◽  
Eiji Kimura ◽  
...  

2019 ◽  
Vol 51 (01) ◽  
pp. 33-36

Choi IJ et al. Helicobacter pylori therapy for the prevention of metachronous gastric cancer. N Engl J Med 2018; 378: 1085–1095


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