Page 108 - Helicobacter pylori and Gastric Cancer: From Tumor microenvironment to Immunotherapy

Introduction
Gastric cancer (GC) remains the second most leading cause of cancer-related deaths and ranks 4th in cancer incidence worldwide[1, 2]. Incidence rates and presentation of gastric cancer show, however, marked regional differences, European countries tend to have a low incidence[3]. In contrast, in Iran for instance stomach cancer together with breast cancer has the highest incidence and highest mortality of all types of oncological disease in this country[4]. In contrast, gastric cancer has a low prevalence in sub- Saharan Africa with the lowest incidence rates in Western Africa[5]. Thus, gastric cancer is constitutes a global health issue, but presentation is markedly different in various parts of the world, raising questions as to whether screening strategies should to be tailored according to geography.
Appropriate screening is important as the prognosis of gastric cancer varies dramatically according to disease stage. The 5-year survival rate for advanced gastric cancer is less than 20%. In contrast, early gastric cancer (EGC) has a good prognosis, with reported 5-year survival rates being in excess of 90 % or even 95 %[5, 6]. The main risk factors for gastric cancer are Helicobacter pylori infection, salt intake, smoking, alcohol, a family history of gastric cancer, atrophic gastritis (AG), and intestinal metaplasia (IM)[7]. Especially AG and IM are important as they are considered to be premalignant lesions of gastric cancer[7, 8]. Hence accurate detection of AG and IM is essential for effective combat of gastric cancer.
AG and IM have multiple etiologies but the most important risk factor for these conditions is Helicobacter pylori infection[9-11] and according H. pylori eradication therapy provides a preventive effect with respect to gastric cancer development[12, 13]. Thus it is especially important to establish that screening for H. pylori- associated is adequate and appropriate irrespective of the geographical context. Currently the gold standard for the diagnosis of AG and IM is histological evaluation of biopsies by the pathologist[14]. In practice, however, in many cases physicians rely on endoscopic evaluation, especially for making a diagnosis of atrophy. Especially the endoscopic atrophy classification (EAC) according to Kimura and Takemoto[15, 16] is frequently been used to evaluate the atrophic degree of gastric mucosa. However, although intraobserver agreement for gastric mucosa atrophy using the Kimura-Takemoto Classification. tends good to excellent, interobserver agreement is moderate even in experienced endoscopists[17], suggesting that histology-free evaluation may be suboptimal. Surprisingly, however,
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