Follow the Metaplasia: Characteristics and Oncogenic Implications of Metaplasia’s Pattern of Spread Throughout the Stomach

Frontiers in Cell and Developmental Biology ◽

10.3389/fcell.2021.741574 ◽

2021 ◽

Vol 9 ◽

Author(s):

José B. Sáenz

Keyword(s):

Gastric Cancer ◽

Chronic Inflammation ◽

Main Product ◽

Human Stomach ◽

Innate Immune ◽

Gastric Epithelium ◽

Epithelial Barrier ◽

Clinical Implications ◽

Immune Organ ◽

Patients At Risk

The human stomach functions as both a digestive and innate immune organ. Its main product, acid, rapidly breaks down ingested products and equally serves as a highly effective microbial filter. The gastric epithelium has evolved mechanisms to appropriately handle the myriad of injurious substances, both exogenous and endogenous, to maintain the epithelial barrier and restore homeostasis. The most significant chronic insult that the stomach must face is Helicobacter pylori (Hp), a stomach-adapted bacterium that can colonize the stomach and induce chronic inflammatory and pre-neoplastic changes. The progression from chronic inflammation to dysplasia relies on the decades-long interplay between this oncobacterium and its gastric host. This review summarizes the functional and molecular regionalization of the stomach at homeostasis and details how chronic inflammation can lead to characteristic alterations in these developmental demarcations, both at the topographic and glandular levels. More importantly, this review illustrates our current understanding of the epithelial mechanisms that underlie the pre-malignant gastric landscape, how Hp adapts to and exploits these changes, and the clinical implications of identifying these changes in order to stratify patients at risk of developing gastric cancer, a leading cause of cancer-related deaths worldwide.

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AMBIVALENCE OF CHRONIC INFLAMMATION IN THE MUSCULOUS STOMACH

Crimea Journal of Experimental and Clinical Medicine ◽

10.37279/2224-6444-2020-10-2-104-111 ◽

2020 ◽

Vol 10 (2) ◽

pp. 104-111

Author(s):

O. V. Shtygasheva ◽

E. S. Ageeva

Keyword(s):

Gastric Cancer ◽

Peptic Ulcer ◽

Gastric Ulcer ◽

Gastric Mucosa ◽

Chronic Inflammation ◽

Morphological Changes ◽

Reference Points ◽

Gastric Epithelium ◽

H Pylori ◽

Cag A

For peptic ulcer disease, the etiological role of H. pylori infection has been proven, 60-90% of gastric cancer cases are associated with H. pylori. The bacterium is recognized as a first-order carcinogen. An association has been established between the successful elimination of H. pylori and a reduced risk of gastric cancer and relapse of peptic ulcer. In the pathogenesis of chronic inflammation in the gastric mucosa associated with H. pylori, there are reference points that determine the further path of development of the pathology. If peptic ulcer is not a consequence of the direct damaging effect of NSAIDs, it is associated with the development of gastritis. In gastric ulcer, gastritis is found in both the antrum and the fundus of the stomach Atrophy of the glands begins in the antrum, then its foci are found in the fundus on the front and back walls. Gradu- ally they increase in size, merge with each other, the acid secreting zone decreases, and the border between the fundus and pyloric glands shifts in the proximal direction. With atrophic fundus gastritis, the likelihood of developing high ulcers and stomach cancer increases. Significant increase in apoptosis processes with relative rigidity of proliferation leads to the formation of ulcer, and carcinogenesis is due to excessive proliferation and accumulation of cell mutations. One of the subjects of damage is Cag A H. pylori protein, which implements remodeling of the gastric epithelial barrier. Among its effects are modulation and impaired proliferation of gastric epithelium, leading to morphological changes. The aggressive action of Cag A protein enhances toxic doses of alcohol and smoking, supporting inflammation and causing damage to the gastric mucosa. Despite the common etiology and pathogenesis of gastric ulcer and gastric cancer, the relationship with the de- velopment of atrophic pangastritis and the similarity of convention risk factors determines that the key point in the manifestation of gastric cancer is a genetic predisposition in the form of gene polymorphism causing severe atrophy as a result of chronic inflammation.

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Ultrastructural Cytochemical Study of Human Gastric Cancer: Observation of AKP ase,ACP ase,G6P ase,TPP ase and CO ase

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100158819 ◽

1990 ◽

Vol 48 (3) ◽

pp. 254-255

Author(s):

Dong Yuming ◽

Yang Guanglin ◽

Du Wei Dong ◽

Xu Ai Liam

Keyword(s):

Gastric Cancer ◽

Gastric Epithelium ◽

Human Gastric Cancer ◽

Electron Microscopic ◽

Cytochemical Study ◽

Electron Microscopic Cytochemistry ◽

Cytochemical Reaction ◽

Set Up ◽

Cancer Tissues ◽

Cytochemical Technique

The activities and distributions of AKPase ,ACPase,G6Pase,TPPase and COase in human normal gastric mucosa and gastric cancer tissues were studied histochemically at light microscopic level. These enzymes are the marker enzymes of cell membrane lysosome endoplasmic reticulum, Golgi apparatus and mitochondrion objectively. On the basis of the research we set up a special ultrastructural cytochemical technique and first researched into gastric cancer domesticly. Ultrastructural cytochemistry is also called electron microscopic cytochemistry. This new technique possesses both the sensitivity of cytochemical reaction andi the high resolution of electron microscope. It is characterized by direct observation,exact localization and the combination morphology with function.The distributions of AKPase,ACPase,G6Pase,TPPase and COase in 14 cases of gastric cancer and 1 case of gastric Denign lesion were studied ultrastructurally. The results showed: 1. normal gastric epithelium had no AKPase reaction. The reaction of ACPase,G6Pase,TPPase and Coase were found in the corresponding organella, which were consistent with their function.

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Helicobacter pylori Outer Membrane Vesicles and Extracellular Vesicles from Helicobacter pylori-Infected Cells in Gastric Disease Development

International Journal of Molecular Sciences ◽

10.3390/ijms22094823 ◽

2021 ◽

Vol 22 (9) ◽

pp. 4823

Author(s):

María Fernanda González ◽

Paula Díaz ◽

Alejandra Sandoval-Bórquez ◽

Daniela Herrera ◽

Andrew F. G. Quest

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Outer Membrane ◽

Extracellular Vesicles ◽

Membrane Vesicles ◽

Outer Membrane Vesicles ◽

Host Cells ◽

Gastric Epithelium ◽

Infected Cells ◽

H Pylori

Extracellular vesicles (EVs) are cell-derived vesicles important in intercellular communication that play an essential role in host-pathogen interactions, spreading pathogen-derived as well as host-derived molecules during infection. Pathogens can induce changes in the composition of EVs derived from the infected cells and use them to manipulate their microenvironment and, for instance, modulate innate and adaptive inflammatory immune responses, both in a stimulatory or suppressive manner. Gastric cancer is one of the leading causes of cancer-related deaths worldwide and infection with Helicobacter pylori (H. pylori) is considered the main risk factor for developing this disease, which is characterized by a strong inflammatory component. EVs released by host cells infected with H. pylori contribute significantly to inflammation, and in doing so promote the development of disease. Additionally, H. pylori liberates vesicles, called outer membrane vesicles (H. pylori-OMVs), which contribute to atrophia and cell transformation in the gastric epithelium. In this review, the participation of both EVs from cells infected with H. pylori and H. pylori-OMVs associated with the development of gastric cancer will be discussed. By deciphering which functions of these external vesicles during H. pylori infection benefit the host or the pathogen, novel treatment strategies may become available to prevent disease.

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