Cancer Research. The Biology of Gastric Cancer


Literature Review, 2017

8 Pages


Excerpt

2
Inhaltsverzeichnis
Introduction ... 3
Biological Changes during Onset and Progression of Gastric Cancer ... 3
Distinctive Characteristics of Cancer Cells ... 5
Effect of Gastric Cancer in the Body ... 5
Therapies for Gastric Cancer ... 6
Lifestyle Changes in Gastric Cancer Prevention and Treatment ... 7
Relationship between Gastric Cancer and other Cancers ... 7
References ... 8

3
Introduction
From a pathological perspective, cancers occur due to the failure of the immune system.
It is evident that the immune system plays key roles in preventing cancer through regulating cell
population in the body (Dicken et al., 2005). Ordinarily, the body's immune system is usually
involved in some cellular processes, especially in the cell cycle in which it destroys old or
defective cells through programmed cell death, a process commonly known as apoptosis. In the
context of cancer, this process is usually impaired, thus damaged or defective cells are not
destroyed by the immune system. In addition, the impairment of the immune system's activity
affects cellular homeostasis processes including irregular cell division. These factors are
responsible for tumor growth and progression of cancer. Gastric cancer affects the digestive
system, primarily the stomach. Anatomically, the stomach occupies the region from the
esophageal junction to the duodenum (Cabebe, 2015). Therefore, aim of this research is to carry
out a comprehensive review of gastric cancer, also known as stomach cancer.
BiologicalChangesduringOnsetandProgressionofGastricCancer
In gastric cancer, biological cellular changes occur due epigenetic modification of genes
involved in maintaining the integrity of cells. These genetic alterations are responsible for
changes in cell structure and behavior. One of the key changes caused by mutations of the key
genes in gastric cells is changes in gene expression. It is apparent that gene alterations influence
the amount of cellular proteins produced by gastric cells. Second, genetic alterations result into
the production of defective or abnormal protein products that do not play their cellular biological
roles or alter the function of other proteins in the cell. In gastric cancer, there are several
molecules which structural alterations. Some of these molecules include the cell cycle regulator
(cyclin E) the apoptosis inhibitor (bcl-2), multifunction protein (beta-Catenin), epidermal growth

4
factor, cell adhesion protein (E-cadherin), and plasmolagen activator. On the other hand, some of
these molecules exhibit alterations in gene expression. For instance, gastric cancer cells exhibit
gene amplification that is responsible for overexpression of K-sam and c-erbB2 proteins which
act as growth factor receptors (Becker, Keller & Hoefler, 2000).
Some of the key genes whose epigenetic modifications lead to the development of gastric
cancer are CDH1 gene, TP53 gene and APC gene. CDH1 regulates the expression E-cadherin of
epithelial cadherin which is involved in cell-cell adhesion, cell movement and cell signaling.
Therefore, gene alterations on CDH1 impair the development of organized tissues due to changes
in cytoskeletal structures. These alterations have also been found to lead to the development of
gastric cancer because it acts as a tumor suppressor gene. On the other hand, mutations on TP53
gene lead to the production of abnormal p53 protein which plays key roles in immune system
surveillance. Clinical investigations reveal that TP53 protein is either lost or damaged in 80
percent of gastric cancers. Finally, alterations in APC gene impairs cell signaling within gastric
cells (Zheng, Wang, Ajani & Xie, 2004).
At the organ level, gastric cancer causes several biological changes. Clinical studies
indicate that noncohesive tumor cells infiltrate the stomach wall. This process leads to glandular
formation that does not function as normal gastric glands. In addition, lesions occur on the
gastric wall in which diffuse tumors cause inflammation and desmoplasia (Dicken, Bigam, Cass,
Mackey, Joy & Hamilton, 2005). Moreover, notch signaling in gastric tumorigenesis appears
specific for gastric cancer (Kim & Shivdasani, 2011).

5
DistinctiveCharacteristicsofCancerCells
In practice, the appearance of tissues and organs is determined by the types and
arrangement of cells that constitute specific tissues or organs. Cancer is usually identified on the
basis of the normal appearance of tissues. Therefore, the distinction between characteristics of
cancer cells and normal cells is paramount in pathological investigations of cancer. From a
pathological perspective, a comprehensive distinction can be guided by three core features; shape
and size of the cells, nucleus appearance and the arrangement of cells in tissues. Ordinarily,
normal cells exhibit consistency in the size and shape. In contrast, cancer cells lack consistency,
they are either smaller or larger than normal cells, and their shapes are distorted due to
cytoskeletal changes. Second, cancer cells have larger and darker nucleus compared to normal
cells. Finally the arrangement of normal cells possesses characteristics which are specific to a
certain tissue or organ. For instance, gastric cells form glands that produce mucus to protect the
gastric wall, digestive enzymes and gastric acid that aid digestion. In contrast, gastric cancer
cells form distorted glands. Another significant difference between normal gastric cells and
gastric cancer cells is that, normal cells are localized implying that they stay within the gastric
walls. This localization is absent in gastric cancer cells because they spread to other surrounding
tissues during the progression of the disease, a phenomenon known as metastasis (Duffy,
McGowan & Gallagher, 2008).
EffectofGastricCancerintheBody
The pathophysiology of gastric cancer explains how the disease affects the body as it
progresses. The enlargement of tumors disrupts stomach distension and bowel obstruction. In
some cases of ulcerative tumors, bleeding occurs, and this is manifested as melena,
gastrointestinal hemorrhage or hematemesis. In advanced gastric cancer, ascites and
Excerpt out of 8 pages

Details

Title
Cancer Research. The Biology of Gastric Cancer
College
Egerton University
Author
Year
2017
Pages
8
Catalog Number
V384370
ISBN (eBook)
9783668626409
ISBN (Book)
9783668626416
File size
491 KB
Language
English
Tags
cancer, research, biology, gastric
Quote paper
Patrick Kimuyu (Author), 2017, Cancer Research. The Biology of Gastric Cancer, Munich, GRIN Verlag, https://www.grin.com/document/384370

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