Search

The human gastrointestinal tract (GI tract) is a distinctive organ occupied by a series of commensal microorganisms, while also being showed to an overwhelming load of antigens in the form of dietary antigens on a daily basis. The GI tract has played dual role in the body, in that it performs uptake of nutrients and digestion while also performing out the complex and principal task of maintaining immune homeostasis, i.e., maintaining the balance between the good and the bad. It is equally important that we protect ourselves from reacting against the good, meaning that we reside tolerant to harmless food, commensal bacteria and self-antigens, as well as react with force against the bad, meaning induction of immune responses against harmful microorganisms. This complex task is achieved through the presence of a highly efficient mucosal barrier and a specialised multifaceted immune system, made up of a large population of scattered immune cells and organised lymphoid tissues termed the gut-associated lymphoid tissue (GALT). This book chapter provides an overview of the primary components of the human mucosal immune system and how the immune responses in the GI tract are coordinated and induced.

The complete human genome sequence published by Celera and Human Genome Project in 2001 has provided us with in-depth knowledge about both location and structure of genes; however, they do not provide any information about the genetic diversity between and within human populations. International associations such as the 1000 genomes project, Simons Genome Diversity Project and International HapMap project employed high-throughput sequencing technologies to explore the genetic diversity among various human population across the world. All these studies suggested that every human endures 250–350 loss-of-function mutations on average as well as they are heterozygous for about 60–120 variants, which are associated with genetic disorders. Information about this genetic diversity among human enable us to carry out genome-wide association studies (GWAS) and recognize genes and its respective variants related with any traits of interest or diseases. Till date, more than 1600 GWAS studies have been reported on ~300 traits and diseases. Gastric cancer is a solid tumor with complex genetic and environmental interactions. Major gastric cancers are adenocarcinomas. Germline disparities of DNA sequence between different ethnic populations make one population more disposed to gastric cancer as compared to others. In this article, we reviewed all genes and its polymorphisms related with early-onset gastric carcinoma. In near future, these identified genetic polymorphisms can be utilized as biomarker in the detection and prevention of gastric cancer.

Cancer progression is a multistep process during which normal cells exhibit molecular changes that culminate into the highly malignant and metastatic phenotype, observed in cancerous tissues. The initiation of cell transformation is generally associated with genetic alterations in normal cells that lead to the loss of intercellular- and/or extracellular-matrix- (ECM-) mediated cell adhesion. Transformed cells undergo rapid multiplication and generate more modifications in adhesion and motility-related molecules which allow them to escape from the original site and acquire invasive characteristics. Integrins, which are multifunctional adhesion receptors, and are present, on normal as well as transformed cells, assist the cells undergoing tumor progression in creating the appropriate environment for their survival, growth, and invasion. In this paper, we have briefly discussed the role of ECM proteins and integrins during cancer progression and described some unique conditions where adhesion-related changes could induce genetic mutations in anchorage-independent tumor model systems.