scholarly journals Gastric Xanthoma Associated with Gastric Cancer Development: An Updated Review

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Faycal Awaleh Moumin ◽  
Abdimajid Ahmed Mohamed ◽  
Abdirahman Ahmed Osman ◽  
Jianting Cai
Keyword(s):  
Gastric Cancer ◽  
Early Gastric Cancer ◽  
Chronic Gastritis ◽  
Incidental Finding ◽  
Predictive Marker ◽  
Cancer Development ◽  
Hyperplastic Polyps ◽  
Benign Lesions ◽  
H Pylori ◽  
Foamy Macrophages

Gastric xanthelasma (GX) is a rare tumor-like lesion customarily found as an incidental finding due to its asymptomatic appearance. Grossly, it is a well-marked yellow-white plaque created in the lamina propria by microscopic clusters of foamy macrophages. Xanthelasma is rarely correlated with gastric hyperplastic polyps; gastric xanthomas are rare benign lesions that appear to be associated with inflammation of the gastric mucosa. Etiopathogenesis is also unclear, but it has been suggested to be involved in chronic gastritis, infection with Helicobacter pylori (H. pylori), diabetes mellitus, and hyperlipidemia. The gastric xanthoma prevalence ranges from 0.23% to 7%. Orth first described the condition in 1887. It has been found that xanthelasmas are associated with chronic gastritis, gastrointestinal anastomosis, intestinal metaplasia, and H. pylori infection. These lesions predispose patients to gastric cancer conditions. Xanthoma (GX) was reported to be a predictive marker for early gastric cancer. However, the effectiveness of these scores and xanthoma (GX) as predictive markers for early gastric cancer detected after H. pylori eradication remains unknown.

scholarly journals Role of TNF-α-Inducing Protein Secreted by Helicobacter pylori as a Tumor Promoter in Gastric Cancer and Emerging Preventive Strategies

Toxins ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 181
Author(s):  
Masami Suganuma ◽  
Tatsuro Watanabe ◽  
Eisaburo Sueoka ◽  
In Kyoung Lim ◽  
Hirota Fujiki
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Cell Surface Receptor ◽  
Tumor Promoter ◽  
Cancer Development ◽  
Human Gastric Cancer ◽  
Tnf Α ◽  
Surface Receptor ◽  
H Pylori ◽  
Factor Α

The tumor necrosis factor-α (TNF-α)-inducing protein (tipα) gene family, comprising Helicobacter pylori membrane protein 1 (hp-mp1) and tipα, has been identified as a tumor promoter, contributing to H. pylori carcinogenicity. Tipα is a unique H. pylori protein with no similarity to other pathogenicity factors, CagA, VacA, and urease. American H. pylori strains cause human gastric cancer, whereas African strains cause gastritis. The presence of Tipα in American and Euro-Asian strains suggests its involvement in human gastric cancer development. Tipα secreted from H. pylori stimulates gastric cancer development by inducing TNF-α, an endogenous tumor promoter, through its interaction with nucleolin, a Tipα receptor. This review covers the following topics: tumor-promoting activity of the Tipα family members HP-MP1 and Tipα, the mechanism underlying this activity of Tipα via binding to the cell-surface receptor, nucleolin, the crystal structure of rdel-Tipα and N-terminal truncated rTipα, inhibition of Tipα-associated gastric carcinogenesis by tumor suppressor B-cell translocation gene 2 (BTG2/TIS21), and new strategies to prevent and treat gastric cancer. Thus, Tipα contributes to the carcinogenicity of H. pylori by a mechanism that differs from those of CagA and VacA.

scholarly journals Helicobacter pyloriAnti-CagA Antibodies: Prevalence in Symptomatic and Asymptomatic Subjects in Turkey

2002 ◽  
Vol 16 (8) ◽  
pp. 527-532 ◽  
Author(s):  
M Fatih Abasiyanik ◽  
Ersan Sander ◽  
Barik A Salih
Keyword(s):  
Gastric Cancer ◽  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Chronic Gastritis ◽  
Molecular Weights ◽  
Cancer Antigens ◽  
Gastroduodenal Disease ◽  
H Pylori ◽  
Asymptomatic Subjects

BACKGROUND: Several reports have shown the prevalence of anti-CagA antibodies to be associated with the development of peptic ulcer diseases, while others have indicated that there is no such association.AIM: To examine the prevalence of antibodies to CagA and otherHelicobacter pyloriantigens in symptomatic and asymptomatic subjects in Turkey.SUBJECTS AND METHODS: Sixty-six symptomatic subjects, 16 to 74 years of age, were examined forH pyloriby biopsy-based tests and ELISA. One hundred nineteen asymptomatic subjects, 20 to 65 years of age, were also tested serologically for the presence ofH pylori. Samples from both groups that were found to be positive forH pyloriby ELISA were then tested by immunoblotting.RESULTS: Fifty-four (82%) symptomatic subjects and 76 (64%) asymptomatic subjects were found to beH pylori-positive by ELISA. Samples from 30 symptomatic subjects who were found to beH pylori-positive by ELISA were analyzed by immunoblotting. Antibodies to CagA (116 kDa) antigen were detected in immunoblots of 11 of 14 (79%) with chronic gastritis, 12 of 13 (92%) with duodenal ulcer and three of three (100%) with gastric cancer. Antigens of the following molecular weights were also detected in these 30 subjects: 89 kDa (VacA) in 21 (70%), 37 kDa in 21 (70%), 35 kDa in 19 (63%), 30 kDa in 27 (90%) and 19.5 kDa in 19 (63%). Immunoblots of 40 ELISA-positive asymptomatic subjects showed that 33 (83%) had antibodies to CagA antigen, 26 (65%) to VacA antigen, 30 (75%) to a 37 kDa antigen, 30 (75%) to a 35 kDa antigen, 39 (98%) to a 30 kDa antigen and 36 (90%) to a 19.5 kDa antigen.CONCLUSIONS: Antibodies to CagA antigen were prevalent in both groups, regardless of the presence of gastroduodenal disease.

scholarly journals Induction and prevention of gastric cancer with combined Helicobacter pylori and capsaicin administration and DFMO treatment, respectively

2020 ◽  
Author(s):  
Faisal Aziz ◽  
Mingxia Xin ◽  
Yunfeng Gao ◽  
Josh Monts ◽  
Kjersten Monson ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Mouse Models ◽  
Chronic Gastritis ◽  
Molecular Mechanisms ◽  
Gastric Carcinogenesis ◽  
Lifestyle Changes ◽  
Host Susceptibility ◽  
Anti Inflammatory ◽  
H Pylori

Abstract Background: Gastric cancer risk evolves over time due to environmental, dietary, and lifestyle changes including Helicobacter pylori (H. pylori) infection and consumption of hot peppers (i.e. capsaicin). H. pylori infection promotes gastric mucosal injury in the early phase of capsaicin exposure. In addition, capsaicin consumption is reported to suppress immune function and increase host susceptibility to microbial infection. This relationship suggests a need to investigate the mechanism of how both H. pylori infection and capsaicin contribute to gastric inflammation and lead to gastric cancer. No previous experimental animal models have been developed to study this dual association. Here we developed a series of mouse models that progress from chronic gastritis to gastric cancer. C57-Balb/c mice were infected with the H. pylori (SS1) strain and then fed capsaicin (0.05% or 0.2g/kg/day) or not. Consequently, we investigated the association between H. pylori infection and capsaicin consumption during the initiation of gastric inflammation and the later development of gastric cancer. Tumor size and phenotype were analyzed to determine the molecular mechanism driving the shift from gastritis to stomach cancer. Gastric carcinogenesis was also prevented in these models using the ornithine decarboxylase inhibitor DFMO (2-difluoromethylornithine). Results: This study provides evidence showing that a combination of H. pylori infection and capsaicin consumption leads to gastric carcinogenesis. The transition from chronic gastritis to gastric cancer is mediated through interleukin-6 (IL-6) stimulation with an incidence rate of 50%. However, this progression can be prevented by treating with anti-inflammatory agents. In particular, we used DFMO to prevent gastric tumorigenesis by reducing inflammation and promoting recovery of disease-free stasis. The anti-inflammatory role of DFMO highlights the injurious effect of inflammation in gastric cancer development and the need to reduce gastric inflammation for cancer prevention. Conclusions: Overall, these mouse models provide reliable systems for analyzing the molecular mechanisms and synergistic effects of H. pylori and capsaicin on human cancer etiology. Accordingly, preventive measures like reduced capsaicin consumption, H. pylori clearance, and DFMO treatment can lessen gastric cancer incidence. Lastly, anti-inflammatory agents like DFMO can play important roles in prevention of inflammation-associated gastric cancer.

A case of chronic gastritis, misdiagnosed as early gastric cancer

1966 ◽  
Vol 1 (3) ◽  
pp. 43-43
Author(s):  
N. Egi ◽  
T. Okuhara ◽  
M. Shibahara ◽  
H. Kodama ◽  
K. Mituta
Keyword(s):  
Gastric Cancer ◽  
Early Gastric Cancer ◽  
Chronic Gastritis

Sa1298 – Gastric Xanthoma is a Useful Predictor for Early Gastric Cancer Detected After H. Pylori Eradication

2019 ◽  
Vol 156 (6) ◽  
pp. S-310
Author(s):  
Narihiro Shibukawa ◽  
Shohei Ouchi ◽  
Shuji Wakamatsu ◽  
Yuhei Wakahara ◽  
Akira Kaneko
Keyword(s):  
Gastric Cancer ◽  
Early Gastric Cancer ◽  
H Pylori

scholarly journals A case of metachronous early gastric cancer was diagnosed 4years after eradication of H. pylori infection

2005 ◽  
Vol 66 (2) ◽  
pp. 54-55
Author(s):  
Mikinori Kataoka ◽  
Takashi Kawai ◽  
Kouhei Kawakami ◽  
Satoru Taira ◽  
Takao Itoi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Early Gastric Cancer ◽  
H Pylori

scholarly journals Predictive Value of CDX2 and SOX2 in Chronic Gastritis and Intestinal-type Gastric Cancer

2020 ◽  
Vol 8 (A) ◽  
pp. 947-955
Author(s):  
Noha Helal ◽  
Zeinab Omran ◽  
Tarek Aboushousha ◽  
Magdy Youssef ◽  
Afkar Badawy ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Chronic Gastritis ◽  
Immunohistochemical Staining ◽  
Therapeutic Interventions ◽  
Intestinal Type ◽  
Intestinal Differentiation ◽  
Cell Lineages ◽  
Sox2 Expression ◽  
Cdx2 Expression ◽  
H Pylori

BACKGROUND: Worldwide gastric cancer (GC) ranks sixth in incidence and second in mortality among all malignancies. CDX2 has an essential role in the development and maintenance of intestinal differentiation in the gut and ectopic sites such as intestinal metaplasia (IM) of the stomach. SOX2 contributes to the cell lineages normally found in the stomach, suggesting contribution in gastric differentiation. AIM: The aim of the study was to assess the expression of CDX2 and SOX2 in chronic gastritis (CG) lesions associated with Helicobacter pylori, IM, or dysplasia as well as in intestinal-type GC. METHODS: Immunohistochemical staining for CDX2 and SOX2 were applied on archival paraffin blocks from 80 CG cases, 40 intestinal-type GC cases, and 10 controls. CG cases were either of non-specific inflammation or associated with H. pylori infection. GC cases were of intestinal-type only, excluding any other type of GC. Control cases were of minimal gastritis, negative for H. pylori, IM, and dysplasia. RESULTS: CDX2 expression was correlated with CG associated with H. pylori, IM, and dysplasia as well as with more differentiated and less invasive pattern of intestinal-type GC, while SOX2 expression was correlated with CG negative for H. pylori and IM as well as with less differentiated and more invasive intestinal-type GC. CONCLUSION: Both CDX2 and SOX2 could predict the behavior of CG disease over time and plan the suitable line of treatment and both proteins could be potential targets for novel therapeutic interventions.

scholarly journals Gastric xanthelasma: case report

2020 ◽  
Vol 7 (2) ◽  
pp. 594
Author(s):  
Ana C. Almeida ◽  
Emília C. Fraga ◽  
Cristina P. Camacho ◽  
Maria J. Amaral ◽  
António Milheiro ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Case Report ◽  
Predictive Marker ◽  
Gastric Antrum ◽  
Complete Regression ◽  
Upper Gi ◽  
H Pylori ◽  
Single Lesion ◽  
Development Of Gastric Cancer

Xanthelasma, also known as Xanthoma or lipid island, is an uncommon gastrointestinal tract (GIT) tumor-like lesion and the stomach is its most frequent location in upper GI lesions, specifically in the gastric antrum, as a single lesion. The pathogenesis appears to be related to healing processes in response to tissue damage provoked by inflammation induced by Helicobacter pylori infection. Many studies have reported that successful H. pylori eradication helps prevent gastric cancer (GC) development. We present a case of a 77 years old patient that showed endoscopic diagnosis of erythematous gastropathy, a gastric antrum xanthelasma and H. Pylori infection. After confirmed H. pylori eradication, the lesion had complete regression. The successful eradication of H. pylori probably led to a total regression of the lesion. Gastric xanthelasma (GX) has been shown to be an independent predictive marker for early GC detection after H. pylori eradication. GX could be a useful marker for predicting the development of gastric cancer.

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