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From Inflammation to Cancer: Role
of Genetic Polymorphisms of Inflammatory
Pathway Molecules in Gastric Cancer
4
Israa Abdullah Malli
Abstract
Gastric cancer is a pathological alteration that affects the cellular lining of the
stomach, causing some of the gastric cells transformed to become malignant cells.
Gastric cancer is still on the top five leading causes of cancer death in both
genders worldwide. During the past decade, new important data indicated that the
prevalence of gastric cancer is changing due to multiple etiology. However,
Helicobacter pylori infection, geographical locations, inflammation, and cancer
subtype, ag e, and environmental changes are reported risk factors that are com-
monly associated with gastric cancer. Helicobacter pylori infection is recognized
as a principal gastric cancer-associated risk due to its direct effects on gastric
tissues. It was reported that it affects cellular cancer formation by increasing
proliferation rate, upregulating inflammatory response and apoptosis. There are
also several human polymorphisms identified and associated with gastric cancer;
most of them occur within immune response genes. This book chapter will
discuss recent pathological and epidemiological aspects from the perspective of
polymorphisms and gastric carcinoma. It will also summarize our understanding
of the genetic basis of gastric cancer, which will be remodeled to the new
recognition of gastric cancer as a multifactorial disease with distinguished patho-
genicity and polymorphism. This understanding will have important implications
in the future of the management and prevent ion of gastric cancer. This chapter
will discuss molecular alterations that have been characterized for GC.
I. A. Malli (*)
Department of Basic Medical Sciences, College of Medicine-Jeddah, King Saud Bin Abdulaziz
University for Health, King Abdulaziz Medical City, Ministry of National Guard—Health Affairs,
Jeddah, Saudi Arabia
e-mail: Mallii@ksau-hs.edu.sa
#
The Author(s), under exclusive license to Springer Nature Singapore Pte
Ltd. 2021
A. S. Sameer et al. (eds.), Genetic Polymorphism and Cancer Susceptibility,
https://doi.org/10.1007/978-981-33-6699-2_4
79
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Keywords
Gastric cancer · Stomach cancer · Gene polymorphism · Polymorphisms ·
Helicobacter pylori
Abbreviations
APCs Antigen-presenting cells
BabA Blood group antigen-binding adhesin
CagA Cytotoxin-associated gene
CGC Cardia gastric cancer
CIMP CpG island methylator phenotype
CIN Chromosomal instability
DLBCL Diffuse large B-cell lymphoma
EMT Epithelial-mesenchymal transition
GAPPS Gastric adenocarcinoma and proximal polyposis of the stomach
GC Gastric cancer
GERD Gastroesophageal reflux disease
GISTs Gastrointestinal stromal tumors
GLP Gastric linitis plastica
HDGC Hereditary diffuse gastric cancer
HNPCC Hereditary nonpolyposis colon cancer
ICCs Interstitial cells of cajal
MALT Mucosa-associated lymphoid tissue
MAPK Microtubule-associated protein kinase
MSI Microsatellite instability
MUC1 Mucin 1
NCGC Non-cardia gastric cancer
NK Natural killer
OipA Outer inflammatory proteins
PGL Primary gastric lymphoma
PMNs Polymorphonuclear cells
SabA Sialic acid-binding adhesin
SNPs Single nucleotide polymorphisms
Tis Carcinoma in situ
TNFα Tumor necrosis factor-alpha
VacA Vacuolating cytotoxin
WHO World Health Organization
80 I. A. Malli
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4.1 Introduction
Gastric cancer is classified among the top most common malignancy that increases
the mortality rate due to cancer around the world (Bray et al. 2018). It is a pathologi-
cal alteration that affects the cellular lining of the stomach, causing the transforma-
tion of some of the gastric cells to become malignant cells (Venerito et al. 2018).
Gastric cancer is considered a civilized disease as it has been associated with the
early development of modernization (Ang and Fock 2014). The first traced cases of
gastric cancer were believed to be reported by Ebers Papyrus. However, the gastric
cancer diagnosis was unknown as the characterization of benign and malignant
tumors was not determined yet (Santoro 2005).
Gastric cancer tends to develop slower than other forms of cancers as
pre-cancerous cellular modifications occur in the mucosa lining of the stomach
over many years before true gastric cancer cells develop and progress. However,
gastric cancer is classified among the most aggressive types of cancers (Mairimclean
et al. 2014). Thus, it is often diagnosed at a later stage, which contributes to its poor
prognosis (Carcas 2014). The global shift toward organic and preservative-free
nutrients is expected to contribute to enhancing gastric cancer prevention and
believed in reducing gastric cancer cases (Correa and Piazuelo 2012). In 2012, the
International Journal of Cancer had estimated 951,000 new cases and 723,000
deaths of gastric cancer (Ferlay et al. 2015).
However, the disease progress rate continued in 2018 and the World Health
Organization (WHO) reports that gastric cancer was expected to be the third
among the most common with 27,600 new cases and 11,010 gastric cancer deaths
in the USA (Jemal et al. 2010). The global estimate of gastric cancer is reported to be
more than 1.22 million new cases, and 865,000 deaths occurred worldwide of gastric
cancer (Etemadi et al. 2020). Gastric cancer is a heterogeneous multifactorial disease
of molecular complexity that demands continued updates and research toward
advancement. Genetic, Helicobacter pylori infection, nutritional factors, and envi-
ronmental factors are common etiology that create some challenges for the diagno-
sis, prevention, and alternative therapeutic solutions of molecular markers (Baniak
et al. 2016; Zamani et al. 2018).
4.1.1 Classifications
4.1.1.1 Histological Classifications
Gastric cancer is considered one of the slow progressing diseases that tend to
develop slowly with no specific signs and symptoms over many years, while
pre-cancerous alteration at the gastric mucosa originates. Based on the type of
affected cells it originates from, gastric cancer can be classified into four types:
adenocarcinoma, primary gastric lymphoma (PGL), carcinoid tumor, and
leiomyosarcoma. Adenocarcinoma arises from columnar glandular epithelium cells
lining of the stomach; it accounts for nearly more than 90% of stomach cancer
(Taghavi et al. 2012).
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Adenocarcinoma
The adenocarcinoma was first classified based on the morphology, growth, and
differentiation of cancer cells until Lauren et al. had reported the histological
based classification of gastric cancer in 1965. According to Lauren’s, gastric cancer
is classified into two main subtypes (Lauren 1965; Van Cutsem et al. 2016). Both
types do not transform into the other because they have defined characteristics and
numerous variations in their origin, etiology, pathology, epidemiology, and behavior
(Carcas 2014). The intestinal gastric cancer is the most common type which is
prevalent in high-risk areas; it is usually associated with high-risk populations,
elderly adult males, it has a better prognosis than diffuse gastric cancer (Yasui
et al. 2011).
Intestinal gastric cancer is caused by the bacteria Helicobacter pylori, which
releases some virulence factors that invade the epithelial cells and cause extensive
cellular damage (Suzuki et al. 2012). It is characterized by metaplasia that originates
from the glandular involvement of adhesive tubular cells that might induce high
vascularity and possible invasion from the lymphatic circulation (Waldum and
Fossmark 2018). On the other hand, the diffuse gastric cancer is characterized by
single non-adhesive cells that infiltrate as scattered small groups of cells (Du 2006).
Despite that, the diffuse type of gastric cancer is more common in low-risk areas and
mostly affecting a much younger female population; it is reported to have a worse
prognosis and short duration compared to the intestinal type (Assumpção et al.
2020).
Primary Gastric Lymphoma
The primary gastric lymphoma (PGL) arises from lymphocytes that are found in the
wall of the stomach. It has two predominant histological subtypes: mucosa-
associated lymphoid tissue (MALT) and diffuse large B-cell lymphoma (DLBCL).
However, gastric lymphoma is considered an uncommon malignancy compared to
adenocarcinoma, and it accounts only for 4% of gastric cancer cases (Hosseini and
Dehghan 2014). B lymphocytes are responsible for recognizing and responding to
any pathogen that crosses the epithelial layer. An excessive B cell proliferation
during a chronic Helicobacter pylori infection makes B cells more prone to having
mutations and developing a diffuse well-differentiated lymphocyte (Juárez-Salcedo
et al. 2018).
Carcinoid Tumor
The carcinoid tumor originates from neuroendocrine cells like the G cells, the
hormone-producing cells of the stomach. This form of gastric tumor accounts for
only 3% of gastric cancer cases and usually localizes without spreading to nearby
organs. Carcinoid tumor causes a well-differentiated mass that protrudes from the
mucosa and appears as a polyp (Nikou and Angelopoulos 2012). It has three types:
Type I and II ECL-cell carcinoids present with little to no symptoms. Thus, it is
usually accidentally discovered during endoscopy. The third type, Type III ECL-cell
carcinoids, is considered the more aggressive type, which presents with more
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pronounced symptoms such as bronchial tube constriction, severe abdominal pain,
and diarrhea (Dias et al. 2017). This form of cancer is not unique to G cells of the
stomach; it can form malignancy at other locations also where G cells are found,
such as in the pancreas and intestine (Oronsky et al. 2017).
Leiomyosarcoma The leiomyosarcoma of gastric cancer arises from stromal
smooth muscle cells that cover the gastric wall. It is considered an extremely rare
type of gastric cancer characterized by undifferentiated cells (Agaimy and Hartmann
2010). Although gastrointestinal stromal tumors (GISTs) are reported to originate
from the interstitial cells of Cajal (ICCs), a specialized cell is located in the
gastrointestinal tract, but it is commonly associated with stomach malignancy
(Kang et al. 2019).
4.1.1.2 Anatomical Classifications
The stomach has five regions: the cardia, the upper part next to the esophagus and
has the esophagogastric junction; the fundus, the second part after the cardia; the
body or the corpus, the main part that connects upper to lower; the pyloric antrum,
the lowest part of the stomach; the pylorus, the last part that has a pyloric sphincter to
be connected to the small intestine (Ellis 2011 ). The first three parts of the stomach
(cardia, fundus, and body) are called the proximal stomach, which is responsible for
digestive enzymes production and intrinsic factor secretion that is needed for vitamin
B12 absorption. The lower two parts are called the distal stomach (Mahadevan
2014). According to the adenocarcinoma location, GC can be classified based on
major topographical subsites into cardia gastric cancer (CGC) and non-cardia gastric
cancer (NCGC) (Hu et al. 2012). Acco rding to 2012 estimates, the worldwide cardia
and non-cardia gastric cancer incidence rates have been reported 260,000 cases of
CGC and 691,000 cases of NCGC. Each type possesses distinct characteristics in
their descriptive epidemiology and risk factors; however, NCGC is more frequent
than CGC, with an average ratio of 2:1 (Colquhoun et al. 2015).
Cardia gastric cancer affects the cardia region, the upper part of the stomach, at
the gastroesophageal junction. CGC is thought to be mainly caused by damage to the
cells at the gastroesophageal junction as a result of chronic irritation of the gastro-
esophageal junction by stomach acidity which leads to gastroesophageal reflux
disease (GERD) (Carr et al. 2013). This CGC is found to be associated with an
increased intake of saturated fat and increased BMI that lead to severe obesity.
Therefore, obesity increases the risk of cardia stomach cancer, but it shows no
association with NCGC (Mukaisho et al. 2015). CGC can be established with or
without Helicobacter pylori infection. If the disease starts independent of
Helicobacter pylori, it manifests after a longstanding mucosal inflammation without
atrophic gastritis, while atrophic gastritis can be observed when it is associated with
Helicobacter pylori infection (Pennathur et al. 2013).
Non-cardia gastric cancer affects the non-cardia region, the main area of the
stomach wall. The non-cardia region of the stomach holds unprocessed food 4–5h
during digestion. Thus, the non-cardia type is affected by the exposure to nutritional
factors such as alcohol consumption, cigarette smoking, food-preservative, and high
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