Journal of Gastrointestinal & Digestive System
Open Access

Gastric carcinogenesis is a complex and multifactorial process, in which infection with Helicobacter pylori is one of many factors that play a significant part in the complicated and multiple process of gastric carcinogenesis. Additionally, the etiology of gastric cancer (GC) is heavily influenced by environmental factors as well as genetic susceptibility factors. Multiple genetic and epigenetic alterations that occur over the course of a cancer patient's lifetime and either activate or inactivate tumor-suppressor pathways lead to the development of gastric cancer.

The main subject of this review will be the molecular phenotypes of GC, which were the subject of numerous research works that were published last year. This article also discusses current discoveries on possible novel genes and GC tumor-suppressor genes. Understanding the fundamental mechanisms behind stomach carcinogenesis will be crucial for creating screening, early diagnosis, and treatment options. The seventh decade of life is the peak for gastric cancer. The bad prognosis is frequently the result of a delayed diagnosis. Fortunately, thorough investigation into the pathophysiology of stomach cancer has led to the discovery of novel risk factors, effective treatments, and cutting-edge endoscopic methods. The way gastric cancer is currently treated has been transformed by the discovery that Helicobacter pylori infection is the primary cause of the majority of stomach ulcers. Adenocarcinoma, non-lymphoma, Hodgkin's and carcinoid tumors are examples of gastric tumours.

Men and women are not equally impacted; male incidence rates are roughly twice as high as female incidence rates. For instance, based on information from the GLOBOCAN database, the cumulative risk for stomach cancer until age 74 was 1.87% for men and 0.79% for women in 2018. The male:female ratio, however, is roughly equal or even displays a female majority among younger people. Early in the development of GC, mutations in the genes encoding the tumour protein p53 (TP53) and catenin (CTNNB1) arise, which contribute to gastric carcinogenesis. Additionally, considerable percentages of GCs exhibit Runx3 loss as a result of hemizygous deletion and promoter hyper methylation. In addition to GC, aberrant Cdx2 expression has been seen in precancerous lesions. It is still unknown, nevertheless, whether Cdx2 contributes to the development of stomach cancer. Microsatellite instability in GC is another clearly identified subpopulation with unique clinico-pathologic characteristics. The prognosis of patients with advanced GC was recently improved by targeted therapy against GC with ERBB2 amplification. Additionally, epigenetic alterations in GC may be desirable targets for modulators used to treat cancer. Gastric cancer (GC) results from a multistep interaction that is impacted by Helicobacter pylori contamination, hereditary vulnerability of the host, as well as of other ecological elements. GC results from the collection of various hereditary and epigenetic modifications in oncogenes and cancer silencer qualities, prompting dysregulation of numerous flagging pathways, which upset the cell cycle and the harmony between cell multiplication and cell passing.

For this unique issue, we have chosen to survey last year's advances connected with three fundamental points: The cell of beginning that starts threatening development in GC, the systems of direct genotoxicity prompted by H. pylori disease, and the job of deviantly communicated long noncoding RNAs in GC change. The comprehension of the atomic premise of GC improvement is of most extreme significance for the ID of novel focuses for GC counteraction and treatment.