The Uncontrolled Proliferation Of Abnormal Cells Biology Essay

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Any type of disease characterised by the uncontrolled proliferation of abnormal cells that grow beyond their natural borders is termed cancer by the World Health Organisation. These cells can affect any tissue of the body, invade surrounding ones and even reach 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.

One of the most significant demographic changes of the 21st century is the aging population. "The ageing process is of course a biological reality which has its own dynamic, largely beyond human control. However, it is also subject to the constructions by which each society makes sense of old age. In the developed world, chronological time plays a paramount role. The age of 60 or 65, roughly equivalent to retirement ages in most developed countries, when they secure their pension entitlement, is said to be the beginning of old age." (Gorman, 1999)

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Cancer is a worldwide disease common to people of all age-groups (Administration on Aging, 2000). Cancer was the leading cause of newly diagnosed disease and death in 2008 with an estimated 12.7 million new cases and 7.6 million death worldwide (Ferlay, 2010). However, incidence and mortality rates are highest in persons aged 60 years and above (Wedding, 2007) thus affecting the elderly population to a greater extent than the younger population. There are a number of possible reasons to explain these findings in the aged population, some of which suggest a considerable amount of genetic damage to cells that has built up over time and an extended exposure to cancer-causing substances over the years (Taylor and Kuchel, 2009).

By the year 2050, the Mauritian elderly population is expected to treble to about 371 000 (Suntoo, 2012). With the expansion of this age group, the absolute number of older individuals diagnosed with cancer in future decades will undoubtedly increase and this situation presents itself as a major challenge for medical professionals.

EPIDEMIOLOGY OF CANCER IN THE ELDERLY

In the United States, 60% of all newly diagnosed cancer patients and 70% of all cancer deaths occur in the elderly population (Rao et al., 2008). According to the National Cancer Registry of the Republic of Mauritius, 40% of all new cases of cancer registered for the period 2005-2008 occurred in the elderly (55% in males and 41% in females). The incidence of cancer amongst the elderly is estimated to rise by about one third over the next three decades (Ferlay, 1999).

INCIDENCE

Following statistics from Cancer Research UK for the year 2005-2008, 53% of all cancers were diagnosed in patients aged between 50 and 74 years of age with slightly more cases in males (an average of 88,198 per year) than in females (78,240) and 36% of all new cancers were diagnosed in patients aged 75 years and above.

MORTALITY

In the UK, for the period 2007-2009, cancer was responsible for 40% of deaths in the 50-74 year olds and 26% of deaths in those aged 75 years and older for males while 47% of females above 50 years old and 18% of females above 75 years died of cancer according to Cancer Research UK.

PATHOGENESIS OF CANCER

Cancer cells are formed when the genetic material or DNA (deoxyribonucleic acid) within the normal cell nucleus gets damaged. DNA is responsible for all cellular activities: growth, death, protein synthesis etc. When DNA is damaged, the cell usually either repairs the damage or dies. In cancer cells, however, neither is the damaged DNA repaired, nor does the cell die. Instead it starts multiplying to give more of such abnormal cells with damaged DNA. Genomic damage may be inherited from parents or may be the result of exposure to certain cancer-causing agents.

THE NORMAL CELL CYCLE

The normal cell cycle consists of 4 main stages: G1, S, G2 and M and represents all structural changes that occur in a cell for mitosis to occur. G1 is the first gap after proliferative stimulus but if the cell is meant to divide, then there are biochemical reactions which occur in G1 to prepare the cell for replication. The S phase is for DNA synthesis and chromosome replication. G2 is the second gap after DNA synthesis. M refers to mitosis stage leading to the breakdown of nuclear membrane and cytokinesis to produce two daughter cells. The last stage G0 involves non-cycling cells in a resting state with G1 DNA. There are also three major checkpoints during the cell cycle: The G1 checkpoint ensures that enough nutrients are available to support the resulting daughter cells; The G2 checkpoint ensures that DNA replication in S phase has been completed successfully; The metaphase checkpoint ensures that all of the chromosomes are attached to the mitotic spindle by a kinetochore.

CANCEROGENESIS

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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:

The first stage - INITIATION involves rapid and irreversible DNA lesion which occurs when a normal human cell encounters a carcinogen. Throughout the initiation, the main changes in cell-regulating mechanisms that occur include proto-oncogenes which code for normal cell growth are converted to oncogenes which cause uncontrolled growth stimulation; Tumour suppressor genes which usually regulate cell proliferation get deactivated; Genome repair mechanisms responsible for screening the DNA for defects and restoring it are non-functioning; Apoptosis regulating mechanisms which cause auto destruction of defective cells are inactive.

The second stage - PROMOTION refers to the prolonged exposure to substances (tumour promoters) which are not directly carcinogenic in their own right but maintain and stabilise the initiated lesion). During this step, tumour promoters contribute to carcinogenesis by activating intracellular signalling pathways to mainly promote clonal cell expansion.

The final stage - PROGRESSION describes the progress to malignancy following further interaction with carcinogens and tumour promoters where there is uncontrolled multiplication, loss of differentiation, local invasion and even metastasis.

CARCINOGENS

Carcinogens (also called mutagens) are cancer-causing substances. 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. For an individual, the probability for developing a cancer following exposure to a particular carcinogen depends on the way the person has been exposed, the length, intensity, type of exposure and genetic factors.

CHEMICAL CARCINOGENS

Everyday people are exposed to chemical compounds with mutagenic properties (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 pathophysiological 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. Compounds containing in tobacco have been proved to exhibit mutagenic properties and cause lung cancer (Hecht, 1999). Aflatoxins, produce by a mold and present in dietary supplies has been recognised to cause primary liver malignancies amongst Africans and Asians (Wogan et al, 2004). Heterocyclic amines are indirect-acting mutagens produced when meats are heated above 180 degrees Celsius for long periods but they must be metabolized to electrophiles in the liver before causing genomic damage.

PHYSICAL CARCINOGENS

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 prostheses), fibres (asbestos) and particulate materials (crystalline sillica) that initiate cancerogenesis mainly through their physical effects on a cell, rather than through chemical interactions with the cell, compared to "chemical carcinogens" (Bast et al, 2000).

The mechanism of cancerogenesis associated with physical mutagens is uncertain. One theory explains that the physical particles initiate a strong inflammatory response in surrounding tissues followed by infiltration of the tissue with the host's immune cells. The host defences being unable to dislodge the foreign particle, this results in chronic inflammation. While the normal tissue continues to undergo proliferation, some cells undergo neoplastic changes. The larger surface area of the particle, the more cells able to come into contact with the particle, the more severe is the inflammation and the higher is the risk of cellular mutation. Bakelite disks initiate local fibro sarcomas (Turner 1942). Studies have proved undeniable mutagenic properties of asbestos fibres on various human (Landrigan, 1991).

Electromagnetic and ionising radiations initiate cancerogenesis through a two-step mechanism. First, the radiation directly ionises cellular molecules. Second, the interaction with cellular water and oxygen produces free radicals which cause genomic breakage, enzyme inactivation and membrane lysis.

BIOLOGICAL CARCINOGENS

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This class of mutagens consists of viruses, bacteria and parasites which have been recognised to innitiate cancerogenesis after infecting the human body. It has been found Hepatitis B, hepatitis C (liver cancer), human papillomavirus (cervical cancer) and Helicobacter pylori (stomach cancer) infections are responsible for up to 18% of cancer burden (Parkin, 2006).

After transferring its genetic material to human cells for replication, a virus can cause genomic deregulation in the host cell can occur via two mechanisms. The viral genome can either form a stable bond with the human genome, after which it is translated into a new combined genome and from then it is involved in cellular mechanisms or it can bind cellular proteins and affect the signal transduction for example Epstein-Barr virus is responsible nasopharyngeal carcinoma and Burkitt's B-cell lymphoma (Bell, 2006).

Bacterial infections and parasitic infections have been found to cause cancer through chronic inflammation as in the case of Helicobacter pylori which causes gastric cancer and Schistosoma haematobium associated associated with high incidence of bladder cancer (Botelho, 2010) but bacteria also produce mutagenic compounds as a result of their metabolic activities (Parsonnet, 1995).

ENDOGENOUS METABOLIC BYPRODUCTS

Normal cellular activities can also be a cause of cancer. Our body metabolism generates a large amount of oxygen reactive species, nitrosamines, and reactive aldehydes. Our detoxification mechanisms usually get rid of these potential carcinogens but not perfectly especially in pathophysiological complications like chronic inflammation. Endogenous DNA damage occurs more frequently than damage by external agents but the types of damage produced by normal cellular processes are very similar to those caused by environmental carcinogens (Jackson and Loeb, 2001)

CANCER RISK FACTORS

Changes in the cell which give rise to cancer occur by varying degrees of interaction between host factors and exogenous factors.

HOST FACTORS

Host factors or endogenous factors arise within the patient's body. These include heredity, hormones (Alvarez, 1982) and age (Kono, 2010).

AGE

Old age is the greatest cancer risk factor (Colditz, et al., 2006). 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). These trends however decline in the oldest (90 years and above) (Agostara et al., 2008).

GENETICS AND CANCER

Patients whose family members have had cancer are more likely to develop cancer themselves. Direct monitoring of patients and their families indicates a hereditary factor in colon, breast, and ovarian cancers, to cite only a few familiar instances. People with a near relative who has had colon cancer are three times as likely to develop it themselves as are people without such a relative (Ramming, 1985). Women whose mothers had breast cancer have three times the risk of contracting this illness as those whose mothers did not have the disease (Newell, 1982).

HORMONES

Endogenous hormones contribute to the development of cancer when they are in excessively high concentrations in the bloodstream. Diseases known or believed to be linked to hormones include cancers of the endometrium, breast, prostate, ovary, testes, thyroid, and bone. The same biological process that promotes normal growth also increases the risk of cancer. Hormones such as testosterone and estrogen promote the growth of tissues in specific "target" organs, such as the prostate and the breast. An excess of hormones accelerates growth, with each extra cell division raising the chance that a cancer cell will be produced (Henderson, 1982). studies have shown that women known to be at risk for breast cancer have elevated levels of estrogen (Henderson, 1975) and that men with prostatic cancer have elevated levels of testosterone (Ghanadian, 1979).

1.4.2 EXOGENOUS AGENTS

These are environmental and behavioural factors which increase the probability for cancer to occur.

DIETARY FACTORS

Our eating habits have a considerable impact on our risk to develop cancer. According to the American Institute for Cancer Research, Food, Nutrition, and the Prevention of Cancer, 375 000 new cancer cases could be prevented yearly through a healthy diet.

Diets containing substantial amounts of red or preserved meats may increase the risk of various cancers, including colorectal cancer. Red meat may be associated with colorectal cancer by contributing to N-nitroso compound (NOC) exposure. Laboratory results have shown that meats cooked at high temperatures contain other potential mutagens in the form of heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs) (Cross,2004).

High fat content is a propable risk factor for cancerogenesis (Khalid, 2009). The association between fat intake and several common cancers, eg, those of the colorectum, breast, endometrium, ovary, and prostate, received its strongest support from correlation studies on populations (La Vecchia, 1992). Strong correlations among countries between per capita dietary fat consumption and rates of cancers of the breast, colon, and rectum have suggested possible causal relationships (Willett, 1998).

One in 20 cancers may be linked to diets low in fruit and vegetables (Parkin, 2011). More than one in ten bowel cancers linked to a low fibre diet (Parkin, 2011). Studies have found that people who eat the most fruit and vegetables can lower their risk of cancer by about a quarter compared to those who eat the least (Benetou, 2008). The UK EPIC study has found that eating lots of fruit and vegetables could reduce the risk of mouth, oesophageal and lung cancers (Boeing, 2006), as well as some types of stomach cancer (Gonzalez, 2006) but have no proven effect on the risk of breast, prostate, ovarian or kidney cancers (IARC, 2003).

TOBACCO AND ALCOHOL

OCCUPATIONAL FACTORS

GEOGRAPHICAL FACTORS

PROTECTIVE FACTORS

1.6 EFFECTS OF TUMOUR ON PATIENT

DETECTION AND DIAGNOSIS

TUMOUR GRADING AND STAGING

Based on the microscopic appearance of cancer cells, pathologists commonly describe tumor grade by four degrees of severity: Grades 1, 2, 3, and 4. The cells of Grade 1 tumors resemble normal cells, and tend to grow and multiply slowly.

The American Joint Committee on Cancer recommends the following guidelines for grading tumours:

Grade

GX Grade cannot be assessed (Undetermined grade)

G1 Well-differentiated (Low grade)

G2 Moderately differentiated (Intermediate grade)

G3 Poorly differentiated (High grade)

G4 Undifferentiated (High grade)

The TNM system is one of the most widely used staging systems. This system has been accepted by the International Union Against Cancer (UICC) and the American Joint Committee on Cancer (AJCC).

The TNM system is based on the extent of the tumor (T), the extent of spread to the lymph nodes (N), and the presence of distant metastasis (M). A number is added to each letter to indicate the size or extent of the primary tumor and the extent of cancer spread.

Primary Tumor (T)

TX Primary tumor cannot be evaluated

T0 No evidence of primary tumor

Tis Carcinoma in situ (CIS; abnormal cells are present but have not spread to neighboring tissue; although not cancer, CIS may become cancer and is sometimes called preinvasive cancer)

T1, T2, T3, T4 Size and/or extent of the primary tumor

Regional Lymph Nodes (N)

NX Regional lymph nodes cannot be evaluated

N0 No regional lymph node involvement

N1, N2, N3 Involvement of regional lymph nodes (number of lymph nodes and/or extent of spread)

Distant Metastasis (M)

MX Distant metastasis cannot be evaluated

M0 No distant metastasis

M1 Distant metastasis is present

TREATMENT