Aurora Kinase A: molecular insights of epstein-barr virus and helicobacter pylori-associated gastric cancer progression

Abstract

Globally, gastric cancer (GC) ranks fourth in terms of cancer-related mortality. In Asia and around the world, it ranks third among female cancer patients and second among male cancer patients [1]. It is the seventh most common cancer among women and the fifth most common among men in India [2]. Gastric cancer signs and symptoms are frequently detected after the disease has progressed, and the 5-year survival rate is less than 30% in developed nations and about 20% in developing nations [3]. The majority of cases of GC now occur in Asia, Latin America, and Central and Eastern Europe; it is no longer a common illness in Western Europe or North America [4]. GC can be distinguished into two types based on the locus, i.e., Gastric adenocarcinomas and gastro-oesophageal junction adenocarcinomas [5]. Lauren's classification further distinguishes between intestinal and diffuse types of gastric adenocarcinomas. Moreover, The Cancer Genome Atlas (TCGA) describes four subtypes of GC i.e., genomically stable (GS), chromosomal instability (CIN), microsatellite instability (MSI), and Epstein-Barr virus (EBV) associated GC (EBVaGC) [6]. Similarly, using a transcriptomic classifier, the Asian Cancer Research Group (ACRG) defined GC into four distinct molecular subtypes: microsatellite instability (MSI), microsatellite stable with epithelial-to-mesenchymal transition features (MSS/EMT), MSS/TP53-active state of TP53 (MSS/TP53+), and MSS/TP53-inactive state of TP53 (MSS/TP53-)