The Cause And Cellular Mechanisms Of Cancer Biology Essay


Cancer (malignant tumour) begins with the genetic alteration of a single cell, leading to continuous proliferation and resulting in an invasive mass that ultimately can kill the organism. Cancer consists of more than 100 types, depends on the location of cell and the genetic aberration in the body. Cancer has such features as uncontrolled cellular proliferation, growth without appropriate signals, ability to escape from apoptosis, intrusion and destruction of adjacent tissues and ability to spread into other locations via lymph/blood (metastasis) (Ecsedy & Hunter 2008).

The transformation from a normal into a malignant tumour cell is a multistage process It is as the result of the interaction between a person’s genetic factors and three categories of external agents: physical carcinogens (UV and ionizing radiation), chemical carcinogens (asbestos, tobacco, aflatoxin, arsenic etc.) and biological carcinogens (certain viruses, bacteria or parasites). It is also believed that as people get older, the higher is the risk of getting cancer. The tendency of cellular repair mechanisms is less effective in aging people (World Health Organization 2011).

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Exposure to ultraviolet radiation (UVR) from the sun is the main cause of skin cancers. Some observations show that skin cancers are more susceptible to whites than blacks. Persons in outdoor occupations and sunny geographic locations are more prone to this type of cancer as well. Ionizing radiation (IR) can induce neoplasia. It is responsible for some cases of skin cancer, leukemia, breast cancer and lung cancer. Larger radiation dose causes cells experience a nonlethal DNA mutation that is passed on to subsequent cell divisions, contributing the formation of a cancer, eg. diagnostic x-rays (Ecsedy & Hunter 2008).

Prolonged exposure to asbestos is the major risk factor for mesothelioma (Trail 2010). Because it is used almost in all industrial products, asbestos may be considered ubiquitous. It is floating in air and traces of mineral have been detected in drinking water, foods, drugs and many others (National Cancer Institute 2002). Tobacco is the main cause of oral and lung cancer. Smoking tobacco as cigarettes exposes the oral and lung cavity to several carcinogens including PAHs, aldehydes and nitrosamines. The risk increases with both the average consumption and duration of smoking (Ecsedy & Hunter 2008). Infectious agents such as viruses, bacteria and parasites account for about 15% of all cancers. Viruses causing cancer (oncovirus) include the hepatitis B and C viruses, the human papilloma viruses and Helicobacer pylori (Parsonnet 1999).

Metastasis is the ability of tumour cells to migrate to distant sites in the body, where the migrating cells take residence and ultimately develop into secondary tumour masses. This makes complete eradication of metastatic cancers extremely difficult and thus accounts for the majority of cancer deaths (Hart & Fidler 1980).

The tumour cells must first detach from neighbouring cells and invade the surrounding stroma (Figure 1). They utilize specialized proteases to destroy the surrounding cell-extracellular matrix membranes that act as migration barriers. The tumour cells then adhere to and enter the endothelial-lined walls of vessels through a process known as intravasation. This allows further proliferation of tumour cells and enlargement of the primary tumour. The cells then migrate via lymph or blood where they lodge and arrest in the capillary bed of organs. They need to survive the mechanical stress and shearing forces of the circulatory flow. Those that survive exit vessel walls (extravasation) and finally, the metastatic tumour cells proliferate into a secondary tumour mass and develop its own vascular network (Ecsedy & Hunter 2008).

Figure 1. The Pathogenesis of Cancer Metastasis (Source: Poste & Fidler 1980).

Only few cells survive the destructive events and form secondary tumour growth. Hart and Fidler (1980) proved that the characteristics of malignant cells might determine the metastasis. They injected cell lines of B16 melanoma tumours to their syngeneic hosts, C5BIJ6 mice. Three weeks later pulmonary metastases were harvested and placed into new tissue cultures. This procedure was repeated few times, and all the tumour lines were assayed. With each successive passage, the incidence of pulmonary metastases increased significantly. This suggested that the survival of tumour cells in the circulatory system depended on unique tumour-cell properties. According to Poste and Fidler (1980), metastases did not result from random survival but from the selective growth of the cells endowed with specific properties that befit them in each step of metastasis process.

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The distribution and viability of circulating tumour cells is influenced by the mechanical factors, such as the size and deformability of tumour cells, the diameter and distensibility of capillaries and the interaction of tumour cells with other circulating cells (Poste & Fidler 1980). Tumour cells that aggregate with other tumour cells (homotypic aggregation), platelets and lymphocytes are the example of the interactions. These can lead to formation of multicellular emboli which can trigger the secondary growth of tumours (Hart & Fidler 1980). Besides, certain tumours are proven to consistently metastasise to particular organs. Why some organs support metastatic growth, while others do not, is still not understood (Poste & Fidler 1980).