Mo1577 Different Protein Expression and Genes Patterns of Helicobater Pylori in Pathological Disorders of the Gastric Mucosa

Re, Vallì De; Repetto, Ombretta; Zanussi, Stefania; Garziera, Marica; Zorzi, Mariangela De; Casarotto, Mariateresa; Giacomini, S.; Basaglia, Giancarlo; Maiero, Stefania; Toffoli, Giuseppe; Canzonieri, Vincenzo; Paoli, Paolo De; Cannizzaro, Renato

doi:10.1016/s0016-5085(12)62432-9

Cited by 1 publication

(2 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Sci. 2020, 21, x FOR PEER REVIEW 2 of 24 the disorder, smoking, exposure to radiation, obesity, underlying medical disorders or (gastroesophageal reflux disease), unhealthy/poor diet, Helicobacter pylori (H. pylori) infection, genetic factors, or prolonged intake of specific drugs such as non-steroidal anti-inflammatory drugs (NSAIDs) or proton-pump inhibitors (PPIs) [9][10][11][12]. Approximately 95% of all GCs incidents are adenocarcinomas, which may arise either from the gastric mucosa or the most superficial glands of the stomach epithelium [13].…”

Section: Epithelial-mesenchymal Transitionmentioning

confidence: 99%

“…Some causative factors may be decisive in the prognosis of patients and further progression of the malignancy. The most common risk factors and predispositions to GC development include belonging to the male gender, old age, family history of the disorder, smoking, exposure to radiation, obesity, underlying medical disorders or malfunctions (gastroesophageal reflux disease), unhealthy/poor diet, Helicobacter pylori (H. pylori) infection, genetic factors, or prolonged intake of specific drugs such as non-steroidal anti-inflammatory drugs (NSAIDs) or proton-pump inhibitors (PPIs) [9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Immunological Aspects of the Tumor Microenvironment and Epithelial-Mesenchymal Transition in Gastric Carcinogenesis

Baj

Brzozowska

Forma

et al. 2020

IJMS

View full text Add to dashboard Cite

Infection with Helicobacter pylori, a Gram-negative, microaerophilic pathogen often results in gastric cancer in a subset of affected individuals. This explains why H. pylori is the only bacterium classified as a class I carcinogen by the World Health Organization. Several studies have pinpointed mechanisms by which H. pylori alters signaling pathways in the host cell to cause diseases. In this article, the authors have reviewed 234 studies conducted over a span of 18 years (2002)(2003)(2004)(2005)(2006)(2007)(2008)(2009)(2010)(2011)(2012)(2013)(2014)(2015)(2016)(2017)(2018)(2019)(2020). The studies investigated the various mechanisms associated with gastric cancer induction. For the past 1.5 years, researchers have discovered new mechanisms contributing to gastric cancer linked to H. pylori etiology. Alongside alteration of the host signaling pathways using oncogenic CagA pathways, H. pylori induce DNA damage in the host and alter the methylation of DNA as a means of perturbing downstream signaling. Also, with H. pylori, several pathways in the host cell are activated, resulting in epithelial-to-mesenchymal transition (EMT), together with the induction of cell proliferation and survival. Studies have shown that H. pylori enhances gastric carcinogenesis via a multifactorial approach. What is intriguing is that most of the targeted mechanisms and pathways appear common with various forms of cancer.EMT refers to the process by which the mesenchymal phenotype is acquired by epithelial cells (ECs) mainly via the reduction of their intracellular adhesions and proliferative capacity (Figure 1.) [47].

show abstract