The WHO defines the term cancer as a group of diseases that can affect any part of the body and which is characterised by the uncontrolled proliferation of abnormal cells that grow beyond their natural borders. These cells can further invade adjoining parts of the body and spread to other organs, through a process called metastasis. The term "cancer" is often used interchangeably with the term "malignant neoplasia" which consists of fast growing poorly differentiated cells invading and destroying tissues of their immediate surrounding and metastasizing in other areas of the human body thereby shortening the life span of the patient, an example being breast adenocarcinoma.
EPIDEMIOLOGY OF CANCER IN THE ELDERLY WORLDWIDE
1.2.3 AGE DISTRBUTION
PATHOPHYSIOLOGY OF CANCER?
THE NORMAL CELL
When a normal human cell becomes cancerous, this transformation is termed cancerogenesis. Cancerogenesis occurs because of damage to the genetic material of the cell upon exposure to carcinogens but this exposure does not immediately lead to malignancy. The process of malignant transformation is divided into three major steps:
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The first stage - INITIATION involves the mutagenic effects of the carcinogens on normal human cell
The second stage - PROMOTION is stimulated by molecules which are not directly carcinogenic in their own right.
The final stage - PROGRESSION describes the progress to malignancy either spontaneously or following further interaction with carcinogens.
Substances and exposures that can lead to cancer are called carcinogens or mutagens. Carcinogens do not cause cancer in every case, all the time. Substances labeled as carcinogens may have different levels of cancer-causing potential. Some may cause cancer only after prolonged, high levels of exposure. And for any particular person, the risk of developing cancer depends on many factors, including how they are exposed to a carcinogen, the length and intensity of the exposure, and the person's genetic makeup. There are four main groups of carcinogens: chemicals, physical agents, viral and bacterial infections and the only way to differentiate between them is the way they cause damage to the genome.
People are continuously exposed exogenously to varying amounts of chemicals that have been shown to have carcinogenic or mutagenic properties in experimental systems (Wogan et al, 2004). They are molecules which form a chemical bond with the human genome and disrupt it. There exist direct-acting physical carcinogens which are already mutagenic before being absorbed by the body and indirect-acting carcinogens which acquire mutagenic properties after having been metabolised by the body. Exposure to these carcinogens can occur exogenously when they are present in food and the environment, but also endogenously when they are produced from bodily activities or pathophysiologic conditions like inflammation (Wogan et al, 2004).
Chemical carcinogens were already described in the year 1775 by Percival Pott who recorded the high incidence of scrotal cancer amongst chimney sweeps due to their constant exposure to coal tars. Tobacco carcinogens and their DNA adducts are central to cancer induction by tobacco products (Hecht, 1999). A causative relationship between exposure to aflatoxin, a strongly carcinogenic mold-produced contaminant of dietary staples in Asia and Africa, and elevated risk for primary liver cancer has been demonstrated through the application of well-validated biomarkers in molecular epidemiology (Wogan et al, 2004). Heterocyclic amines are indirect-acting mutagens produced when meats are heated above 180 degrees Celcius for long periods but they must be metabolized by the family of cytochrome P450 enzymes to chemically reactive electrophiles before reacting with DNA to initiate a carcinogenic response.
The term "physical carcinogens" includes a wide range of agents the most common being, electromagnetic ultraviolet radiations, ionising atomic radiation and materials such as gels (silicone gels in breast protheses), fibres (asbestos) and particulate materials (crystalline sillica) that initiate cancerogenesis mainly through their physical properties and physical effects, rather than through their chemical properties and actions, as opposed to "chemical carcinogens" (Bast et al, 2000). Bakelite disks initiate local fibro sarcomas (Turner 1942). The carcinogenic effect of asbestos fibers of different types on various tissues and organs, both in humans and in experimental animals, is now definitively established by a large number of clinical, epidemiologic, and experimental studies (Landrigan, 1991)
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The biochemical mechanisms of cancer development associated with physical agents is uncertain, and several different theories exist. One theory holds that the physical particles cause irritation in the surrounding tissue, resulting in inflammation. The body's normal inflammatory response involved proliferation of surrounding cells and infiltration of the tissue with new cells. As the particle remains in place and the normal tissue continues to undergo proliferation, some cells mutate into neoplastic (cancer) cells. This idea is supported by studies showing particles of asbestos and erionite with larger surface area to have a higher risk of cancer; the larger surface area is thought to allow more cells to come into contact with the particle, leading to more inflammation. This theoretically results in chronic inflammation and increased risk of cellular mutation.
Electromagnetic and ionising radiations initiate cancerogenesis through a two-step mechanism. First, the radiation directly ionises cellular molecules and thn the interaction with cellular water and oxygen leads to free radical production which damages the genome (chromosomal breakage) and other cellular structures (enzyme inactivation and membrane damage). Bakelite disks initiate local fibro sarcomas (Turner 1942). The carcinogenic effect of asbestos fibers of different types on various tissues and organs, both in humans and in experimental animals, is now definitively established by a large number of clinical, epidemiologic, and experimental studies (Landrigan, 1991)
Viral infection can cause an oncogenic impact because for replication viruses transfer their genetic material into the host's cell. During the transfer, genome deregulation can occur via two main mechanisms:
When implanted into the human genome, the viral genome can bind into a stable form with the human genome, translated into the human genome and from then on be involved onto cellular mechanisms.
The viral genome can bind cellular protein and affect the signal transduction
The following viruses have been recognised to be carcinogenic in humans:
Epstein-Barr virus is responsible Nasopharyngeal Carcinoma and Burkitt Lumphoma.
Human Papilloma virus induces Cervical Cancer, Skin Cancer and Larynx Papilloma
Hepatitits B virus causes induce Hepatocellular Carcinoma
CANCER CAUSES AND RISK FACTORS
Changes in the cell which give rise to cancer occur by varying degrees of interaction between host factors and external agents.
1.4.1 GENETICS AND CANCER
1.4.2 EXOGENOUS AGENTS
Cancer is a worldwide disease common for people of all age-groups (Adminastration on Aging, 2000). The risk of cancer amongst the elderly population is about 10 times more important than in the younger age-group (Yancik, 1997a; Yancik and Ries, 2004). 60% of all cancers have been said to occur in the older age-group (Yancik, 1997b; Hansen, 1998).The incidence and mortality rates of human cancer increase dramatically with age, most likely due to long-term exposure to carcinogenic substances combined with the accumulation of damage to cells and genes over the years and less effective cellular repair mechanisms as a person grows older (WHO, 2012). These trends however decline in the oldest (90 years and above) (Agostara et al., 2008).