We Would All Eventually Develop Cancer If We Lived Long Enough - Essay Example

We Would All Eventually Develop Cancer, If We Lived Long Enough Introduction Cancer refers to a group of diseases characterized by uncontrolled growth of cells. Research has identified more than 100 types of cancer, based on the type of cells initially affected by the diseases (4). Essentially, cancer entails cells getting damaged after an out-of-control cell growth, which then forms masses of tissues referred to as tumors. However, a unique form of cancer, which causes leukemia, hinders the normal functioning of cells through abnormal cell division in the blood stream (5). Cancer is caused by damages or mutations in DNA, carcinogens such as tobacco, asbestos, arsenic, harmful radiations such as gamma and X-rays, sun’s rays and carcinogens from fossil fuel fumes (9). The other causes are genetic predisposition inherited from families and medical factors such as certain viruses linked to cancer including human papillomavirus, which causes cervical cancer, hepatitis B and C and which cause liver cancer (7). Based on what cancer is and its causative agents, this paper tackles the questions of whether or not everybody will eventually get cancer at some point in their lives. With supportive evidence from scientific cancer studies, this paper takes a stance not everyone eventually gets cancer, including those who live long lives. Incidence rates for all types of cancers have increased for all age groups in Great Britain since the mid-1970s. However, the largest increase has been in the 75+ age bracket. The rise has been smaller in the other age groups with the 25-49 registering the smallest increases of 31% between 1975 and 1977 and 2009 and 2011. Table 1: Increases in cancer incidences per age groups in UK since 2000. Age (yrs) Rate per 100,000 people 1975 1985 1995 2005 2011 0-39 2 4 6 7 10 40-59 260 265 270 280 300 60-74 1000 1200 1250 1350 1450 Above 74 1700 2000 2250 2400 2450 Graph 1: Cases of cancer per year and age-specific incidences in 100,000 people in the UK (Retrieved from http://www.cancerresearchuk.org/cancer-info/cancerstats/incidence/age/). Not Everyone Will Get Cancer Although many factors cause cancer, people should not be misled that everyone will get cancer. Not everyone does. The interactions of factors of cancer make the basis of this discussion. The first factor is risky behaviour, by which people indulge in dangerous behaviours that predispose them to cancer or increase their cancer risks (6). These behaviours include smoking, excessive consumption of alcohol, bad or an unhealthy diet (10). In other words, people who take better care of themselves compared to their more careless counterparts are not likely to get cancer, regardless of how long they live since the type of lifestyle a person lives has real and far-reaching consequences on their propensity to get cancer. The table below shows the observed and projected lifetime risks of contracting or being diagnosed with all types of cancers in the UK. Table: The Lifetime Risk of Being Diagnosed with Cancer, UK 2000-2015. Year Percentage Risk Male Female Average Risk 2000 38 34 36 2005 41 39 40 2010 44 40 42 2015 projection 46 41 43.5 Paradoxically, whereas some people take good care of their lives really well and still get cancer others who seem not to care at all and never get cancer. This situation is caused by a person’s genetic predisposition to cancer. In simple terms, genetic predisposition implies to the extent to which an individual’s genetic makeup increases his or her risks of contracting cancer. This genetic predisposition issue has led to the emergence of the concept of cancer families, which have considerably higher cases of cancer compared to other families in a population. Families may be predisposed to a certain type of cancer or different types of cancer, mainly caused by a mutation in their gene (7 & 5). Chance also plays a key role in predisposing some people to cancer than others. For example, many of the gene mutations that predispose people to cancer happen by chance (1 & 2). Whenever cells divide, they have to copy their genetic code completely, a process that is sometimes shrouded by mistakes. While in some cases the mistakes are fatal and end in the death of the daughter cells, some cases have the damages repaired (1 & 2). In addition, some mutations result in little or no difference in the viability and functionality of the cell. An individual’s immune system also plays a significant role in predisposing them to cancer. Age also plays a key role. For instance, health care practitioners say that if all men lived long enough they would get prostate cancer (1 & 2). Reasons thus abound, which attempt to explain the reasons every year, millions of people are diagnosed with cancer while the remaining billions do not suffer from the condition. In fact, in every three people, two never get cancer. What is more, most of heavy smokers do not get cancer. A study conducted by George Klein, Professor Emeritus at the Microbiology and Tumor Biology Center at the Karolinska Institute in Stockholm, Sweden, attempted to highlight this often overlooked fact. At the end, the researcher suggests that more studies ought to aim at unearthing the reasons rather many people are able to resist the dreaded disease. In this study entitled “Toward a Genetics of Cancer Resistance,” which was published in the Proceedings of the National Academy of Sciences, the researcher emphasises the existence of evidences of several biological cancer resistance mechanisms in some people, which decrease their risks of developing cancer. Ostensibly, the suffering that cancer patients and their families and loved ones undergo is the main driving force for scientists who study cancer to explore the idea of the genetics of cancer susceptibility. However, scientists have consistently ignored the genetics of how many people have managed to keep cancer away despite the many risk factors. The most likely reason for this scenario is the belief that once mutation in a specific gene is responsible for cancer, then lack of or no occurrence of the mutation makes other not to get the disease (5). Klein thus opines that a deeper look should be taken with regards to resistance to cancer. For instance, the billions of cancer-free people may have several mechanisms by which they protect themselves from cancer (5). One of the identified anti-cancer mechanisms is immunological in nature. This mechanism has been established to be effective against virus-associated cancer (8). The second mechanism of cancer resistance is genetic, especially DNA repair mechanisms. There are people with variations in the efficiency of DNA repair, an example of which is the specific DNA repair deficiency called xeroderma pigmentosum (5). People with this condition are considerably highly sensitive to ultraviolet light. The other anticancer mechanisms are intracellular and intercellular in nature. Cells trigger apoptosis and other forms of programmed cell death as a component of intracellular defenses against infections (5). This type of defense response is often observed in cases of extensive DNA damage. The aim of such a response it to prevent the host cell from reproducing and spreading to other cells and tissues. However, in some cases, apoptosis and other programmed cell death mechanisms such as pyroptosis and autophagy are not initiated when needed. Such a scenario is encountered in people with the genetically mutated tumor suppressor p53, who have a higher risk of inheriting Li-Fraumeni syndrome. This syndrome is a rare disease in which patients develop multiple tumors (5). In intercellular surveillance, adjacent cells may detect precancerous conditions or activities in neighbouring cells. In collaboration, these neighbouring cells form a micro-environmental control system that works against the development and progression of unhealthy and cancerous cells Contrary Opinion Other groups are undecided on whether everyone will eventually get cancer if they lived long enough. Thus, their response is maybe.’ There are theories used to support the notion that maybe everyone who lives long enough might get cancer (4). One reason for this stance is that the DNA changes that predispose people to cancer must affect both copies of genes for cancer to develop. Thus, one mutation is never enough to cause cancer and a person must already have one DNA change to develop cancer. This situation is normally observed in cancer families. For instance, for breast cancer families, one of two copies of a gene like BRCA1 or BRCA2 may already have DNA damage or change (10). The bottom line of the argument put forward by this school of thought is that if all people programmed to die at some time, then by people living longer that programming has somehow been changed. Presumably, people would get DNA mutations at the current rate, making all people predisposed to cancer if they lived long enough. Therefore, at the initial stages of living long, decreasing the chances of DNA damage would be easier than reprogramming cells by stopping smoking, excessive alcohol consumption and eat fewer calories rather than reprogramming all body cells (10). When cells are programmed to last longer, more people are likely to get cancer. Hence, as more people live longer, they will probably get cancer. References 1. Brenner D, Hall J. Computed tomography—an increasing source of radiation exposure. N. Engl. J. Med. 2007. 357(22): 2277–84. 2. Brenner H, Rothenbacher D, Arndt V. Epidemiology of stomach cancer. Methods of Molecular Biology. 2009; 472: 467–77. 3. Cleaver J, Mitchell, D. Ultraviolet radiation carcinogenesis, fifth edition. Hamilton, Ontario: B.C. Decker; 2000. 4. Freedman A. Follicular lymphoma: 2012 update on diagnosis and management." American Journal of Hematology. 2012; 87(10): 988–95. 5. Klein G. Toward genetics of cancer resistance. PNAS. 2009; 106(3); 859-863. 6. Kravchenko J, Akushevich I, Manton, K. Cancer mortality and morbidity patterns in the U. S. population: an interdisciplinary approach. Berlin: Springer; 2009. 7. Lertkhachonsuk A, Yip H, Khuhaprema T. Cancer prevention in Asia: resource-stratified guidelines from the Asian oncology summit 2013. Lancet Oncology. 2013; 14(12): e497–507. 8. Nastoupil L, Rose C, Flowers C. Diffuse large B-cell lymphoma: current treatment approaches. Oncology. 2012; 26(5): 488–95. 9. Pagano J, Raab-Traub N, Roizman B. Infectious agents and cancer: criteria for a causal relation. Seminar on Cancer Biology. 2004; 14(6): 453–71. 10. Proctor R. The global smoking epidemic: a history and status report. Clinical Lung Cancer. 2004; 5(6): 371–6. Read More