Helicobacter Pylori as a Promoter of Accelerated Regeneration, Pathological Differentiation and Transformation of Normal Gastric Mucosa into Cancerous Type (original) (raw)

Gastric carcinogenesis

Langenbeck's Archives of Surgery, 2011

Introduction In most patients, gastric cancer is diagnosed in advanced stage. Curative treatment options are limited and the mortality is high. The process of gastric carcinogenesis is triggered by Helicobacter pylori-driven gastritis and is further characterized by its complexity of interaction with other risk factors. Health care systems are challenged for the improvement of prevention, early diagnosis, and effective treatments. Methods An extensive literature research has been performed to elucidate the interplay between etiological factors involved in gastric carcinogenesis. Results H. pylori is the most important carcinogen for gastric adenocarcinoma. Evidence is provided by experiments including animal studies as well as clinical observational and interventional studies in humans. Eradication has the potential to prevent gastric cancer and offers the greatest benefit if performed before premalignant changes of the gastric mucosa have occurred. Bacterial virulence factors are essential players in modulating the immune response involved in the initiation of the carcinogenesis in the stomach. Host genetic factors contribute to the regulation of the inflammatory response and in the aggravation of mucosal damage. The harmful role of environmental factors is restricted to salt intake and smoking of tobacco. The ingestion of fruit and vegetables has some protective effect. Conclusion Infection with H. pylori is the major risk factor for gastric cancer development, and thus, eradication of the Helicobacter offers a promising best option for prevention of the disease. Bacterial virulence, host genetic factors, and environmental influences are interacting in the multifactorial process of gastric carcinogenesis.

From Gastric Inflammation to Gastric Cancer

Digestive Diseases, 2010

The majority of gastric adenocarcinomas are related to chronic inflammation induced by Helicobacter pylori infection. For intestinal-type gastric cancer, a multistep process of mucosal alterations leading from gastritis via glandular atrophy, intestinal metaplasia and dysplasia to invasive carcinoma is well recognized. Ongoing clinical studies focus on a 'point of no return'. It is defined as a situation when certain alterations are no longer reversible by H. pylori eradication and progression to gastric cancer may continue. H. pylori affects the mucosal as well as the systemic immune response by secretion of cytokines and the recruitment of distinct inflammatory cells. The immune response is characterized by a balance between a Th1-dominated response and the recruitment of antigen-specific regulatory T cells that allow the bacteria to persist in human gastric mucosa. Besides immune-mediated effects, H. pylori induces cellular alterations as well as genetic alterations in genes that are essential for the epigenetic integrity and mucosal homeostasis. These genetic alterations during gastric cancer development are in focus of intensive research and should ultimately allow the identification of risk factors involved in gastric carcinogenesis. The detection of individuals at high risk for gastric cancer would help to design appropriate strategies for prevention and surveillance.

Gastric cancer, Helicobacter pylori infection and other risk factors

World journal of gastrointestinal oncology, 2010

Gastric cancer incidence is declining. However, it is too early to consider this neoplastic disease as rare and the worldwide mortality rate still remains high. Several risk factors have been identified for non-cardia gastric cancer and primary prevention is feasible since most of the risk factors can be removed. Helicobacter pylori eradication treatment reduces but does not abolish gastric cancer risk. Indeed, gastric cancer is a multifactorial disease and removing one factor does not therefore prevent all cases. Endoscopic surveillance is still needed, especially in subjects at higher risk. The definition of high-risk patients will be the future challenge as well as identifying the best surveillance strategy for such patients.

Clinicopathological Study of Gastric Carcinoma with Special Reference to Helicobacter pylori

Journal of Pure and Applied Microbiology

Gastric cancer (GC) is one of the most common malignancies. Although Helicobacter pylori (H. pylori) is being recognized as a Type I carcinogen for GC and primary gastric lymphoma (PGL), yet many studies especially from the Indian subcontinent do not show any such association. The aim of the study was to evaluate the clinicopathological characteristics of gastric adenocarcinoma and to determine the association of H. pylori infection. This prospective study included 50 cases of histologically proven gastric adenocarcinoma. A detailed clinical history, physical examination and upper gastrointestinal endoscopy were done in all the cases and mucosal biopsies were taken from the growth and the surrounding mucosa. Rapid urease test (RUT) was done to diagnose H. pylori infection. 50 patients of functional dyspepsia were taken as controls. GC was more common in males (70%). The maximum cases were recorded in elderly persons, mostly from 5 th to 6 th decades. Anorexia (60%), dyspepsia (54%) and weight loss (24%) were the commonest clinical presentation. Most of the patients presented within 3-12 month of onset of symptom. In majority of cases, the lesion was confined to the antrum (62%) and body (26%) of the stomach. H. pylori infection was more commonly isolated from the antrum. H. pylori infection was not significantly associated with GC as compared to patients with functional dyspepsia. No association was found between H. pylori infection and gastric carcinoma. Probably gastric cancer is multifactorial disease where dietary, genetic and environmental factors play contributing roles.

Helicobacter pylori infection in gastric cancerogenesis

Journal of Physiology and Pharmacology an Official Journal of the Polish Physiological Society, 2009

Gastric cancer (GS) remains one of the most common cancers worldwide. It is considered as the second most frequent cause of cancer death worldwide, although much geographical variation in incidence exists. Many studies before linked Helicobacter pylori (Hp) which is now considered as an important pathogen, to the risk of developing noncardia GS. This overview attempts to summarize the recent basic and clinical evidence on the link between H. pylori and gastric cancer, after the award of the Nobel Prize for Physiology or Medicine to Drs. J.R. Warren and B.J. Marshall for the first culture and isolation of Hp and the investigation of their relevance to peptic ulcer disease. It become evident that Hp eradication by antibiotic treatment combined with proton pump inhibitor (PPI) serves as the primary chemoprevention strategy to reduce gastric cancer incidence. Moreover, the eradication therapy reduces gastric cancer incidence in patients without any precancerous lesions at the baseline and is most effective before the development of atrophic gastritis. Due to understanding the molecular nature of GC which has been nowadays under intense investigation, our review attempts to highlight recent progress in the field of research on Hp-induced GS. We discuss the geographical diversity in Hp infection and cancer incidence and the mechanistic role of gastrin, cyclooxygenase-2 (COX-2), growth factor, nitric oxide (NO)/NO synthase and E-cadherin/beta-cathenin systems, apoptosis and angiogenesis in Hp-induced gastric carcinogenesis. In addition host-related genetic susceptibility and the role of overexpression of a proinflammatory cytokines and their polymorphism is discussed in the relation to the cascade of events such as gastric atrophy, intestinal metaplasia and dysplasia that finally lead to adenocarcinoma.

Incidence of gastric cancer, its subtypes, and correlation with Helicobacter Pylori

Journal of Pathology of Nepal, 2013

Background: Gastric cancer is the fourth most commonly diagnosed cancer and the second most common cause of cancer related death worldwide. It is the common cause of cancer related death in Nepal. Helicobacter Pylori has been classified as a definite carcinogen along with other factors. The aim of this study was to fi nd the incidence of gastric cancer among the patients undergoing upper gastroscopy, its various subtypes and association with Helicobacter Pylori. Materials and Methods: This is a retrospective and prospective study carried out at GRP Polyclinic and Kist Medical College Teaching Hospital. All the patients undergoing upper gastrointestinal endoscopy were included in this study. Data of all the gastric endoscopic biopsies done from June 2011 to January 2013 were collected and analyzed. All the biopsy specimens were processed routinely in histopathology laboratory. Specimens showing carcinoma were enrolled in this study and all the relevant demographic data were collected...

Update on Gastric Cancer Epidemiology and Risk Factors

Journal of Cancer Therapy

Gastric adenocarcinoma is the most common gastric tumor. It is the fifth most common cancer worldwide after lung cancer, breast, colo rectal and prostate cancer. Long considered enigmatic, its epidemiology has changed over time. In fact, the incidence of distal gastric cancer has declined while that of the cardia was stable or increased. This cancer is multifactorial but reducing the incidence of distal cancer is particularly attributed to advances in the treatment of H. pylori infection. In this review, we analyzed the available data concerning the changing epidemiology of gastric cancer and the main risk factors. The incidence of distal cancer is definitely declining due to the control of Helicobacter pylori infection. Proximal gastric cancer and cardia cancer is particularly due to smoking, overweight.